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Reproductive > Things I don't know: Ob/gyn > Flashcards

Things I don't know: Ob/gyn Flashcards

1
Q

When and from what to germ cells originate?

A

4th week of embryonic life

endoderm of yolk sac

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2
Q

When/how do germ cells form primitive gonad?

A

6th week embryonic life

germ cells migrate to genital ridge and associate with somatic cells

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3
Q

What type of errors occur in older men vs. older women?

A

men: mitotic errors
women: chromosome errors

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4
Q

How does the number of sperm produced differ from the number of ova?

A

sperm: many millions, ongoing process after puberty
eggs: 2.5 million at birth (already have all you will make at this point), most degenerate, left with about 400 ova in reproductive years

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5
Q

When do oogonia

  1. begin meiosis I
  2. what phase does meiosis I arrest
  3. when is meiosis I complete
  4. what phase does meiosis II arrest
  5. when is meiosis II complete
A
  1. month 3 of embryonic development
  2. prophase: diakinesis stage (as primary oocyte)
  3. ovulation
  4. metaphase (as secondary oocyte)
  5. fertilization
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6
Q

What separates?
Are the products identical or different (ignoring recombination)?
What would be the chromosome result be if nondisjunction occurred and a trisomy child was born?
1. Meiosis I
2. Meiosis II

A
  1. homologs; different; all 3 chromosomes are different
  2. sister chromatids; identical; 2 chromosomes match (look at centromeric DNA that is not involved in crossing over), 1 is different
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7
Q

order of mitosis/meiosis

A

Prophase
Metaphase
Anaphase
Telophase

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8
Q

leptotene

A

1st stage prophase

chromosomes have replicated but lie on top of each other

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9
Q

zygotene

A

2nd stage prophase

homologous pairs move together and pair or synapse

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10
Q

pachytene

A

3rd stage prophase
first time you can see bivalent chromosome: CHEERLEADER pose
2 homologous chromosomes now look like a tetrad

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11
Q

diplotene

A

4th stage prophase

CROSSING OVER occurs at CHIASMATA

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12
Q

diakinesis

A

5th stage prophase

oogenesis is frozen here until ovulation

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13
Q

chiasmata

A

areas of contact between homologs allowing crossing over

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14
Q

metaphase

A

nuclear membrane disappears
spindles appear
pairs align on metaphase plate

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15
Q

anaphase

A

homologs/sister chromatids pulled apart by spindles attached to centromeres

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16
Q

telophase/cytokinesis

A

cell division

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17
Q

When does nondisjunction occur?

What will be the status of the chromosomes if a trisomy child is born of it?

A

Meiosis I

all chromosomes are different

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18
Q

Insl-3 (insulin-like substance 3)

A

produced by gonad

play role in testicular descent

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19
Q

If a child has streak gonads or no SRY gene (regardless if XX or XY), what will they look like?

A

no AMH: uterus, fallopian tubes

presents at female with no breasts or periods

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20
Q

Common findings in people with mullein duct abnormalities (MDA)

A

infertility
endometriosis
renal anomalies

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21
Q

When does the uterovaginal septum resorb?

A

9-12 weeks gestation

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22
Q

unicornate uterus

  1. uterus
  2. ovaries
  3. kidneys
  4. pregnancy considerations
A
  1. development of only one horn of uterus
  2. two
  3. ipsilateral (same side) renal anomalies
  4. pregnancy: normal outcome, preterm labor, malpresentation
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23
Q

uterus didelphys

  1. uterus
  2. ovaries
  3. kidneys
  4. pregnancy considerations
A

complete failure of duct fusion

  1. two: separate uteri, upper vagina (lower may be separated by septum), cervizes
  2. two
  3. renal AGENESIS
  4. normal, preterm
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24
Q

T shaped uterus

A

DES exposure in utero

risk for clear cell carcinoma of vagina and pregnancy loss

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25
Q

Rokitansky Kunster Hauser syndrome

  1. uterus
  2. ovaries
  3. kidneys
  4. pregnancy considerations
A

complete agencies of Mullerian structures
present: amenorrhea
1. NO upper vagina, cervix, uterus or tubes
2. 2 (has breast development)
3. anomalies, skeletal anomalies (bifid vertebra)
4. infertility
Tx: create neovagina

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26
Q

imperforate hymen

A

failure of reabsorption of uterovaginal septum
presentation: amenorrhea, cyclic pain, abdominal mass
Tx: hymenotomy (sew it open)

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27
Q

Risk factors you wouldn’t think of for ectopic

A

IVF

endometriosis

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28
Q

Dx and Tx unstable ectopic

A

Dx: blood in abdomen, acute abdomen, blood loss (tachycardia, hypotension, anemia)
Tx: blood type and laparotomy

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29
Q

Dx and Tx stable ectopic

A

counsel about rupture
1. quantitative hCG: normally would double in 48 hours
2. progesterone: less than 5 means failed pregnancy
48 hours later
3. curette uterus: products of conception mean SAB; none mean ectopic
Tx: laparoscopy or METHOTREXATE

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30
Q

progesterone less than 5

A

FAILED pregnancy

ectopic of spontaneous abortion

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31
Q

When is methotrexate appropriate to Tx ectopic? What do you need to do after Tx?

A
  1. mass smaller than 5cm
  2. no cardiac activity
    must follow up with hCG to see if it was effective
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32
Q

What is important to advise ectopic patients of?

A

RECURRENCE
usually other tube is damaged too
discuss contraception, infertility

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33
Q

heterotopic pregnancy

A

RARE

ectopic and IUP at same time

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34
Q

anovulatory cycle

A

plenty of estrogen, insufficient progesterone
most common: peripubertal, perimenopausal
Sx: irregular sometimes heavy bleeding

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35
Q

menstrual irregularity peripubertal

A

REASSURE
no need for exam
Tx: OCs, cyclic progesterone, depo-provera

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36
Q

menstrual irregularity in perimenopausal

A

likely anovulatory bleeding: reassurance (near menopause), progestin replacement
must RULE OUT CA

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37
Q

string of pearls on ovary US

A

PCOS

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38
Q

Tx of PCOS

  1. general
  2. want regular periods
  3. decrease unwanted hair
  4. get pregnant
A
  1. LOSE WEIGHT
  2. OCs
  3. OCs, dipilatories
  4. ovulatory agents, metformin
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39
Q

Other causes of irregular bleeding

A
  1. pregnant: ALWAYS get pregnancy test
  2. anorexia
  3. premature ovarian insufficiency
  4. hypothyroid
  5. hyperprolactinemia
  6. cervical/endometrial CA/polyp
  7. cervicitis
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40
Q

Tx of irregular bleeding in perimenopausal

A
  1. replace hormone: progestin (OCPs, medroxyprogesterone, mirena IUD)
  2. when medicine fails: endometrial ablation, hysterectomy
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41
Q

Tx of leimyomata

  1. asymptomatic
  2. menorrhagia, anemia
  3. Sx of pressure or infertility and want to preserve fertility
  4. severe bleeding, pain, child-bearing over
A
  1. no Tx
  2. NSAIDs, hormones
  3. myomectomy
  4. hysterectomy
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42
Q

indications that irregular bleeding might be CA

A
  1. menometrorrhagia, any post-menopausal bleeding

2. older than 45 (sooner if Hx of anovulatory cycles)

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43
Q

ruling out CA as cause of irregular bleeding

A
  1. PAP
  2. endometrial biopsy: simple hyperplasia give progestins, atypia: hysterectomy
  3. US
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44
Q

PGF2alpha

A

elevated in dysmenorrhea

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45
Q

PGE2

A

elevated in dysmenorrhea

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46
Q

What happens upon infusion of PG to the uterus?

A

uterine contractions and pain

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47
Q

dysmenorrhea

A

due to elevated PGs due to fall in progesterone after luteal phase
Tx: NSAIDs, OCs (prevent ovulation and progesterone interactions)

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48
Q

what is the level of PG in women who do not ovulate and have no dysmenorrhea

A

low

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49
Q

causes of secondary dysmenorrhea

A

PID
endometriosis
ovarian cysts
Tx: tx cause

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50
Q

Tx of endometriosis

  1. first
  2. if no relief
  3. large endometrioma
  4. pain/infertility
  5. mild IVF with difficulties getting pregnant
A
  1. OCPs/depo-provera, NSAIDs started 2 days before menses
  2. laproscopy for Dx: REQUIRES a biopsy
  3. laparotomy and mass removal; hysterectomy if done child bearing
  4. laparoscopy to fulgarate lesions with cautery or laser
  5. IVF
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51
Q

How often do infertile couples present with signs of endometriosis?

A

30-40%

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52
Q

premenstrual syndrome (PMS)

A

cause is unclear, Tx Sx
only occurs in OVULATORY women
Sx regularly occur during the same phase of menstrual cycle and regress rest of cycle
Sx: dysmenorrhea, bloat, weight gain, irritable, difficulty concentrating, tired, moody
Dx: menstrual and Sx diary
Tx: NSAID (dysmenorrhea), diuretics (bloat), OCs, reduce salt, SSRI (mood)

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53
Q

Premenstrual dysphoric disorder (PMDD)

A

extreme PMS: likely an UNDERLYING BEHAVIORAL HEALTH ISSUE that worsens in premenstrual period
PMS Sx plus one of the following: sadness or hopelessness, anxiety or tension, extreme moodiness, marked irritability or anger
Tx: SSRI, OCPs, regular exercise and proper diet, nutritional supplements, avoid stressors

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54
Q

What percentage of pregnancy ends in loss?
When is pregnancy loss more likely to occur?
What percentage is lost after heartbeat is found on US?

A

25% end in loss; most sporadic
earlier pregnancy is at higher risk
once heartbeat is seen: greater than 90% chance of successful pregnancy

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55
Q

most common cause of sporadic pregnancy loss

A

most common: chromosomal abnormalities
most common type of chromosome abnormality: aneuploidy: trisomy 16 followed by 21
single most common abnormality: 45,X

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56
Q

causes and Tx of recurrent pregnancy loss

A
  1. insufficient cervix; cerclage
  2. uterine anomalies; Sx
  3. Ab syndrome; heparin through pregnancy
  4. parent carrier of balanced translocation; prenatal Dx or PGD
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57
Q

insufficient cervix

A

cervical integrity compromised
2nd trimester loss, painless bleeding not associated with contractions
Tx: cerclage placed during first trimester (stitch to keep cervix closed)
treat all subsequent pregnancies after first occurrence

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58
Q

Normal pregnancy presentation

  1. is it normal to bless in 1st trimester
  2. US: transabdominal
  3. US: transvaginal
  4. progesterone level
  5. hCG level
A
  1. 1/4 experience; bleeding with cramping is worrisome
  2. detect gestations when hCG reaches 2000
  3. detects gestational sac when hCG is 1000
  4. progesterone greater than 5
  5. double every 48 hours
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59
Q

prenatal care

A
  1. family Hx questionnaire
  2. discussion of age, medical, medication and drug risks
  3. offer screens
  4. US recommended
  5. further counseling, referrals, tests if indicated
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60
Q

types of congenital anomalies

A
  1. chromosomal: associated with maternal age
  2. single gene: sickle cell, CF
  3. structural: sporadic or teratogen associated
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61
Q

When should all women have an US for detection of congenital anomalies?

A

18-20 weeks

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62
Q
  1. two things that increase chance of multiple gestations
  2. other risk factors
  3. do these apply to monozygotic twinning
A
  1. IVF, advanced maternal age
  2. black, maternal family Hx, young maternal age
  3. only IVF
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63
Q

complications with twins

A
  1. premature: avg. delivery 36 weeks
  2. birth defects
  3. c-section needed for some
  4. maternal DM, hemorrhage
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64
Q

malpresentation

A

requires c-section

includes presentation of any of these first: breech, face, foot, arm, cord, placenta

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65
Q

Dx of IUGR
cause:
1. symmetrical
2. asymmetrical

A

serial US: small for gestational age

  1. chromosomal
  2. smoking, maternal disease causing placental insufficiency
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66
Q

causes for large for gestational age (LGA)

A

maternal DM

also: some birth defects (Beckwith-Weideman)

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67
Q

maternal DM effects on fetus

  1. at risk for at birth
  2. complications
A

LGA (glucose moves across placenta: babies become big)

  1. birth injury: shoulder dystocia
  2. hypoglycemia, polycythemia, hypocalcemia, hyperbilirubinemia
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68
Q

twin twin transfusion

A

monochorionic/diamniotic (MONOZYGOTIC)
one twin receives more nutrients and often one dies
recipient twin: struggle more than donor (CHF, polycythemia)

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69
Q

Whose blood is lost

  1. placenta previa
  2. vaso previa
A
  1. maternal

2. fetal

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70
Q

random facts

  1. should you do a pelvic exam on someone with 3rd trimester bleeding
  2. can you diagnose abruptio placenta on US? placenta previa?
A
  1. NO: could cause hemorrhage

2. NOT: abruptio placenta, YES placentia previa

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71
Q

Mirena

A

IUD with levonorgesterol: thickens cervical mucus and prevents implantation
only LOCAL acting steroidal contraceptive
every 5 years
failure rate: 0.2%
benefits: amenorrhea
EXPENSIVE

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72
Q

Cu IUD

A 
every 10 years
Cu is a spermacide
failure: 0.8%
AE: dysmenorrhea, heavy periods
CI: Wilson's, Cu allergy
MOST EFFECTIVE emergency contraception: prevents implantation (all pregnancies not just implantation)
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73
Q

Least effective to most effective contraception

A
  1. condoms
  2. OCs
  3. depo provera
  4. Cu IUD
  5. mirena and skyla
  6. nexplanon
    LARCs work better
74
Q

condoms

A

only contraception that protects against STI
ALWAYS use
user failure: 21%

75
Q

combination OCs

A

estrogen: stabilize endometrium for regular menses
progesterone: neg. feedback prevents pregnancy (AE vary according to progestin)
non-contraceptive benefits: treat cramps, acne, heavy bleeding; prevent PID (but more likely to have cervicitis) and CA (endometrial, ovarian, colon; NO increase in breast CA)
AE: nausea, irregular bleeding, thromboembolic
user failure: 9%

76
Q

depo provera

A

medroxyprogesterone: neg. feedback on FSH,LH
IM every 12 weeks
user failure: 6%
benefits: no menses
AE: weight gain, more likely to contract HIV from partner (thins vagina)
BBW: bone loss: must come off in 3 years

77
Q

skyla

A

like mirena but for 3 years

for nulliparous, younger patients

78
Q

past IUD concerns vs. current

A

PAST: risk of infections, PID with infertility
braided string, left in for decades
CURRENT: slick string so bacteria can’t get up: SAFE, can give to nulliparous women, teens, those with past Hx of STI and PID
still have to culture for GC and chlamydia (don’t take it out, just Tx infection)

79
Q

nexplanon

A

3 years
failure: 0.05%
AE: irregular menses

80
Q

long acting reversible contraception (LARC) benefits

A

IUD, implant
insert and forget it
highly effective few CI
decrease unwanted pregnancy rates in teens and medicaid

81
Q

contraception preference for someone with previous DVT

A

progestin only: mirena or depo

82
Q

CI for estrogen contraceptives like OCs

A
  1. smoking and over 35 years (in younger patient give it to them and tell them to quit smoking)
  2. liver disease
  3. cardiac disease
  4. breast CA
  5. irregular undiagnosed bleeding
83
Q

How does estrogen cause clots?

Highest risks?

A

increase platelets and decreases ATIII

highest risk: PREGNANCY, oral contraceptives

84
Q

tubal ligation

A 
req. hospital and anesthesia 
sterilization
between pregnancies: laparoscopic
during Cesarean
vaginal birth: umbilical incision
failure: 0.5% first year; 1/100 pregnancy if follow out 10 years and include ectopic
85
Q

tubal occlusion (essure)

A

can be done in clinic
scarring causes occlusion
new AE: rash, hair falling out, bleeding

86
Q

Plan B

A

levonorgestral
must be 16 years or older, expensive
within 72 hours of unprotected sex
decrease risk for 8% to 2%

87
Q

male sterilization

A

office visit
ligation of vas deferent
failure: 0.15%
more easily reversed than female sterilization

88
Q

zona pelucida

A

becomes impenetrable after fertilization so no other sperm can get in

89
Q

blastocyst
fate of
1. inner cell mass
2. outer layer of cells

A

morula cavitates

  1. becomes fetus
  2. become trophoblasts
90
Q

implantation of embryo

A

travels thru uterine cavity and hatches
implants: day 8-9
trophoblastic cells invade decidua

91
Q

trophoblast

A

invades decidua

produces hCG

92
Q

decidua

A

promoted by progesterone produced by corpus luteum

glycogen and lipid rich layer of endometrium

93
Q

estimated due date/date of delivery: EDD

A

count back 3 months from first day of LMP and add 7 days

94
Q

normal gestation time

A

40 weeks +/- 2 weeks

95
Q

first trimester

A

0-14 weeks since LMP

96
Q

second trimester

A

14-28 weeks since LMP

97
Q

third trimester

A

28-40 weeks since LMP

98
Q

abortion

A

less than 20 weeks since LMP or less than 500gm

99
Q

viability

A

greater than 23 weeks since LMP

100
Q

preterm

A

less than 37 weeks since LMP

101
Q

late term

A

greater than 41 weeks since LMP

102
Q

postterm

A

greater than 42 weeks since LMP

103
Q

gravid

104
Q

parity

A

had a baby (dead or alive)

105
Q

abortion

A

previable pregnancy loss: spontaneous or induced

106
Q

G?P??a?b?c
?: numbers
what do each mean

A 
G: pregnancies
P: full term delivery
a: preterm delivery
b: abortion/miscarriages
c: living children
107
Q

When can hCG be detected in pregnancy (weeks and amount)
1. serum
2. urine
What should levels do in pregnancy? When do they peak

A
  1. greater than 5 mIU/ml; 3 weeks gestation (from LMP)
  2. greater than 25 mIU/ml; 5-6 weeks gestation (from LMP)
    double every 48 hours in early pregnancy
    peak: 10-12 weeks
108
Q

When can you first perceive fetal movement?

A

1st pregnancy: 18 weeks

G2 or greater: 16 weeks

109
Q

PE of pregnancy

  1. uterus
  2. cervix
  3. fetal heart tones
A
  1. soft at 6-7 weeks, enlarged at 7-8 weeks
  2. blue and engorged with blood
  3. 10 weeks
110
Q

uterus landmarks in pregnancy

  1. 12 weeks
  2. 20 weeks
  3. after that
A
  1. pelvic brim
  2. umbilicus
  3. once centimeter from pubic bone is one week gestation (goes up)
111
Q

US dating

  1. transvaginal
  2. abdominal
A

gestational weeks

  1. 3-4 weeks; hCG 1000-2000
  2. 5-6 weeks, cardiac activity; hCG 4000-5000
112
Q

first prenatal visit: labs

  1. routine
  2. optional
A
  1. CBC (anemia, thrombocytopenia), urine culture, blood group, infectious disease profile (syphilis, Hep B and C, chlamydia, GC)
  2. HIV (opt out), pap smear, genetic screening
113
Q

Rh (D) antigen

  1. AD or recessive
  2. Ab formed
A
  1. autosomal dominant

2. IgG: crosses placenta

114
Q
  1. pathology of Rh- mom and Rh + fetus
  2. results in?
  3. signs of failure on US
  4. what can be done if Ab are already formed?
A
  1. Ab-antigen complexes on fetal RBC
  2. HEMOLYSIS, HYDROPS FETALIS, high output HF
  3. edema, fetal tachycardia
  4. intrauterine transfusion, early delivery
115
Q

What anti-D Ab titer would be concerning in pregnant mom?

A

8 fold increase

116
Q

prenatal visits

  1. early
  2. 18-20 weeks
  3. 28 weeks
  4. 36 weeks
  5. at birth
A
  1. US for dating; prescribe vitamins (folic acid should be started before); avoid sushi, improve diet
  2. US for anomalies
  3. one hour post Glucola serum glucose: screen for DM; Rhogam if Rh -
  4. repeat STI screen, culture for group B strep
  5. Rhogam if Rh-, penicillin if GBS pos.
117
Q 
how often do prenatal visits occur
1. first visit to 28 weeks
2. 28- 36 weeks
3. 36 wks to delivery
what in general is being addressed at each visit
A
  1. q 4 weeks
  2. q 2 weeks
  3. q 1 week
    address: BP, complaints, FHTs, fundal height, EDUCATION
118
Q

Signs of labor

A

contractions
rupture membranes
bleeding

119
Q

What causes labor in

  1. mammals
  2. humans
A
  1. fetal cortisol increases to threshold, estrogen and progesterone fall, signals PGs
  2. not clear; fetus born with/out rise in cortisol; PGs if given do produce labor though
120
Q

latent phase of labor
How long in
1. primigravida
2. multiparous

A

not in labor to 4-6cm
contractions become regular, painful, cervical dilation picks up
1. may be 18 hours
2. may be very rapid

121
Q

active phase of labor
How fast should it go in
1. primigravida
2. multiparous

A

4-5cm to delivery
1. 0.8 cm/hr
2. 1.3cm/hr
do NOT push until fully dilated: 10cm

122
Q

cervix effacement

A 
thinning of cervix
NOT dilation (happens prior to cervical dilation)
123
Q

ruptured membranes
discharge?
c-section?

A

don’t discharge: RISK of INFECTION

do NOT indicate C-section

124
Q

3 stages of active phase of labor

A
  1. from 4-6cm to completely dilated
  2. completely dilated to delivery
  3. delivery of baby to delivery of placenta
125
Q

Why should you not give oral fluids in labor?

A

risk of aspiration if need anesthesia

126
Q

vaginal birth

  1. place
  2. recovery time
  3. blood loss
  4. episiotomy
  5. where is baby after delivery before mom is discharged
A
  1. labor/delivery/recovery room
  2. 24-36 hours, discharge
  3. 500cc
  4. no
  5. with mom
127
Q

C-section indications

A
  1. malpresentation
  2. failure to descend, dilate (in active labor: 0.8-1.3cm/hr)
  3. abnormal fetal heart tones
  4. birth defects
  5. previous c-section
  6. triplets or higher order
  7. active HSV
  8. HIV
  9. placenta previa
128
Q

c-section

  1. place
  2. recovery time
  3. blood loss
  4. what else do they need?
A
  1. Sx room
  2. 24-48 hrs
  3. 1000cc
  4. ANTIBIOTICS
129
Q

c-section complications

A
  1. hemorrhage
  2. surgical injury to bladder/bowel or infection
  3. adhesions
  4. need for repeat CD in future
130
Q

station of presentation

  1. neg.
  2. 0
  3. pos.
A

cm above or below ischial spine
-5 (beginning) to +5 (time for delivery)
1. neg.: baby has dropped but hasn’t settled into pelvis
2. 0: before descent but in pelvis (lowest baby can get before full dilation)
3. pos.: descent of baby through pelvic canal
don’t push before stage 0

131
Q

lochia

A

vaginal bleeding/discharge persists 3-8 weeks postpartum

132
Q

What might a heavy bleed at day 7-14 postpartum be?

A

shedding of Eschar at placental site

133
Q

postpartum depression
Sx?
risks?
Tx?

A

due to withdrawal of hormones at delivery
Sx: crying, helpless, exaggerated worry about baby, sleeplessness
risks: previous episode, inner city, preterm baby, adolescent mother
Tx: SSRI, breast feed, freq. OB visit, hospitalization sometimes necessary
8 weeks pp Sx remitted

134
Q

postpartum blues

A

realization that life is forever changed, frustration with new duties and lack of support

135
Q

Edinburgh depression scale

A

determines postpartum depression

often given by pediatrician

136
Q

Pregnancy effects on breast

  1. progesterone
  2. estrogen
  3. hPL (placental lactogen)
A
  1. growth of alveoli and lobes
  2. stimulate duct system to grow and differentiate
  3. breast, nipple, areola growth
137
Q

benefits of breast feeding

  1. to infant
  2. to mom
A
  1. immunity (IgA/G/M), nutrition, bonding, protect against allergies/asthma/obesity
  2. natural contraception, weight loss, bonding, protect against breast CA
138
Q

How does PRL work to promote milk production?

A
  1. transcription of casein mRNA
  2. stimulate synthesis fo alpha-lactalbumin
  3. increase lipoprotein synthesis
139
Q

alpha-lactalbumin

A

syn. by PRL

regulatory protein of lactose synthetase

140
Q

oxytocin effects (besides milk let down)

A
  1. increase GI mobility and absorption

2. bonding

141
Q

colostrum
compare to mature milk
1. rich in what
2. less of what

A

first few days of nursing
low volume, high nutritional content
1. rich in: protein, vit. A, NaCl, GFs, antimicrobial factors, Ab
2. less: carbs, lipids, K

142
Q

breast milk

A

glucose
also: amino acids, minerals, lipids (lipids rise through nursing episode)
nursing increases blood flow to breast: increase CO and vasodilation
Maternal diet variation: does NOT cause variation in milk components

143
Q

What should you do in a mom that is worried she isn’t producing enough milk in the first few days postpartum?

A

reassure mom: it’s colostrum

do NOT supplement formula: will stop producing milk

144
Q

def. and causes of chronic pelvic pain

A

DAILY pain (can be worse around menses)
1. endometriosis
2. PID
3. leiomyomata
4. ovarian cysts RARELY cause pain (same with fibroids unless large)
5. adhesions
often hard to pinpoint so GI, GU and musculoskeletal causes can be confused with it

145
Q

Clues that chronic pain is

  1. endometriosis
  2. GI
  3. GU
  4. PID
  5. adhesions
  6. NM
A
  1. in 30s; cyclic, dyspareunia
  2. diarrhea, constipation
  3. frequency or pain when urinating
  4. rather acute, bilateral (exam reveals tenderness)
  5. Hx. of Sx or PID
  6. pain with moving or lifting
146
Q

Chronic pelvic pain workup

A

Hx, physical, US

last resort: laparoscopy (may detect endometriosis, adhesions)

147
Q

Chronic pelvic pain Tx

A

NEVER start narcotics for chronic pain: can get addicted
AVOID: laparotomy (leads to adhesions that cause pain and more Sx cycle)
Requires a TEAM: Gyn, Uro, PT, pain management center, Psych
no known cause: sympathy, counsel. laparoscopy can be therapeutic: women get better if told pelvis is ok
non-narcotic pain meds for NM pain

148
Q

somatization

  1. define
  2. what should you do first
  3. associations
  4. hints that this is somatization
  5. besides symtoms, what else might the patient express
A

psychiatric Dx

  1. expresses emotional distress in form of somatic pain: OFTEN chronic pelvic pain
  2. make it clear you believe they have pain
  3. associated with: physical, emotional, sexual abuse
  4. distress out of proportion to PE findings; multiple shifting somatic complaints at different times in life
  5. anxiety and pain about the Sx
149
Q

adenomyosis Tx

A

first line: OCPs (prevent ovulation), NSAID

severe: hysterectomy

150
Q

dyspareunia

  1. on insertion
  2. on deep penetration
  3. after sex
  4. nonspecific complaint or nothing on exam
A

pain with intercourse
need to know what part of sex, onset, if interfering with relationship
1. vaginitis, vulvitis, vaginal atrophy, vestibular adenitis (can detect inflammation and reproduce discomfort on exam)
2. cervicitis, endometriosis, adhesions, PID, mass effect of fibroids, bladder neck? (can reproduce on exam)
3. contractions
4. ask more questions, may need to refer to specialist, may need education on positions, empathy between partners, couples therapy

151
Q

epididymis

A

stores, protects, and promotes maturation of spermatozoa, recycles damaged sperm

152
Q

ductus (vas) deferens

A

movement of spermatozoa from the epididymis

153
Q

seminal glands

A

secretes seminal fluid: 60% of semen volume

fructose, PGs, enzymes

154
Q

prostate gland

A

secretions make up 30% of semen

155
Q

bulbourethral gland

A

secretes alkaline mucus that help to neutralize acids in vagina

156
Q

detumescence

A

anti-erectile
sympathetic thoracolumbar: T10-L2
occurs as cGMP is degraded by PDE5 in erection

157
Q

tumescence

A

erection
PNS: S2-4
cGMP: NO

158
Q

absolute prereqs for erection

A
  1. adequate arterial flow

2. sufficient nitric oxide synthase to produce NO

159
Q

causes of decreased libido

A
  1. meds, alcohol
  2. depression, fatigue
  3. relationship problems
  4. systemic illness
  5. testosterone deficiency
160
Q

causes of ED

A
  1. vascular: ED can be a sign of CV disease
  2. neurologic
  3. local penile
  4. drugs
  5. hormones
  6. psychological
161
Q

best predictors of ED

A

DM, smoking, HTN, obesity, dyslipidemia, CV disease, meds

162
Q

what suggests psychogenic cause of ED

A
  1. one night couldn’t perform, followed by persistent ED
  2. nocturnal or early mooring erections
  3. inability to maintain erection once penetrated the vagina (can have other reasons)
163
Q

Tx of erectile dysfunction

A
  1. PDE5 inhibitors
  2. alprostadil suppositories
  3. intracavernosal vasoactive drug injection
  4. vacuum erection device
  5. penile prosthesis Sx
164
Q

premature ejaculation

A

brief ejaculatory latency, lack of control of ejaculation, distress in patient or partner
Tx: couples therapy, behavioral approach, manual techniques, topical anesthetics in condom, SSRI

165
Q

retrograde ejaculation

  1. caused by
  2. described/present as
  3. Dx
A

ejaculate semen into bladder

  1. bladder neck damage (in prostate Sx), alpha adrenergic block
  2. dry ejaculate, infertility
  3. low vol. ejaculation with ample sperm count in post ejaculation urine
166
Q 
hematospermia
differential and what to do
1. under 40
2. with ongoing lower urinary tract symptoms
3. older
A

blood in semen

  1. usually benign and self-limited; nothing
  2. infection; urinalysis, culture, studies for STI
  3. prostate CA: referral or CA evaluation
167
Q

genetic potential growth (MPH)

  1. boys
  2. girls
  3. SD
A
  1. boys: (dad height + mom height + 13cm)/2
  2. girls: (dad heigh - 13cm + mom height)/2
  3. SD: +/- 10cm (4in)
    can sub 5.07in for 13cm
168
Q

average height velocities

  1. age 3
  2. age 10
  3. peak pubertal growth spurt
A
  1. 8cm/year
  2. 5cm/year
  3. 10cm/year
169
Q

orchidometer

  1. blue
  2. yellow
A
  1. blue: 1-3cc: prepubertal

2. yellow: 4-20cc: pubertal

170
Q

factors that play a role in GnRH suppression

A
  1. GnRH
  2. NPY
  3. GABA
  4. Leptin
  5. TGF-alpha
171
Q

What two things increase at puberty in response to GnRH? What do they cause to happen

A

kisspeptin and GPR54

stimulate FSH and LH

172
Q

genetic factors controlling puberty

A 
GnGHR
KAL-1
FGFR-1
GPR54
LHX3
173
Q

What effect do these have on H-P-G axis

  1. GABA
  2. glutamate
A
  1. inhibit

2. stimulate

174
Q

GH-IGF

A

affects onset and tempo of puberty

175
Q

routes of signaling in pubertal control

  1. post. hypothalamus
  2. anterior hypothalamus
A
  1. inhibitory

2. stimulatory

176
Q

leptin and puberty

what happens in deficiency

A

acts on hypothalamus
reduces appetite and stimulate gonadotropin secretion
deficiency: obese and gonadotropin deficiency
excess: down regulation of GnRH release

177
Q

tanner stages of testicular enlargement

A

I: smaller than 4cc and 2.5cm
II: growth to 4cc or greater in volume; scrotum reddens and changes in texture
III: enlargement of penis (length first); further growth of testes (10cc)
IV: increased penis breadth and development of glans; scrotum darkens, testes (16cc) and scrotum larger
V: adult genitalia (25cc)

178
Q

lower age limit of tanner stage II

A

AA: 8 years (avg. 11)

white, mexican: 9 years (avg. 12)

179
Q

adrenarche

A

growth spurt, axillary and pubic hair growth; NO sexual development
change in adrenal response to ACTH
rise in hydroxypregnenlone and DHEA relative to cortisol
DHEA greater than 40

180
Q

constitutional delay

A

more common in boys
age of onset of puberty delayed
girls: 2.5 years
boys: 3 years

Reproductive (12 decks)

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