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OBGYN > MedEd Videos > Flashcards

MedEd Videos Flashcards

1
Q

Physiology of pregnancy:

what happens to:

1) MAP
2) SVR
3) HR
4) SV
5) DL CO2
6) Hgb

A

1) MAP –> DECREASE
2) SVR –> DECREASE
3) HR –> 15% increase
4) SV –> INCREASE PRELOAD, no change in contractility
5) DL CO2 –> INCREASE (more RBCs)
6) Hgb –> increase RBCs, but BIG INCREASE in PLASMA (overall decrease in Hgb)

MAP = CO x SVR
CO = HR x SV
SV = preload and contractility
DLCO2 = CO x Hgb x %SaO2
Hgb = [RBC]/[Plasma]
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2
Q

Physiology of pregnancy:

what happens to:

1) Minute Ventilation
2) FEV1
3) PaO2
4) FRC

A

1) Minute Ventilation –> INCREASE Tidal Volume = increase MV (no change in RR)
2) FEV1 –> no change
3) PaO2 –> no change
4) FRC –> DECREASE

Minute ventilation = TV x RR

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3
Q

Physiology of pregnancy:

what factors are increased in the clotting cascade? decreased?

A

1) increase vWF
2) Increase factor 7, 8, 10
3) increase inhibitors of tPA
4) decrease in protein C and S

OVERALL INCREASE IN CLOTTING

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4
Q

Physiology of pregnancy:

what is a normal Cr?
what can happen because of significantly increased GFR during pregnancy?

A

Cr = 0.4-0.8

Significantly increased GFR –> obstructive uropathy at pelvic rim

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5
Q

What is normal weight gain during pregnancy?

A

1) BMI < 18.5 –> 1 lb/wk = 28-40 lbs
2) BMI 18.5-25 –> 0.75 lb/wk = 25-35 lbs
3) BMI 25-30 –> 0.5 lb/wk = 15-25 lbs
4) BMI > 30 –> 0.25 lb/wk = 10-20 lbs

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6
Q

What are GI side effects of pregnancy?

how to treat them? (5)

A

1) GERD –> PPO
2) Nausea –> ondansetron
3) constipation –> stool softeners + motility agents
4) Iron deficiency –> iron supplement + stool softener
5) Gallbladder disease –> remove in 2nd trimester unless emergent

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7
Q

Downs
Edwards
Patau

chromosome?

A 
Downs = 21
Edwards = 18
Patau = 13
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8
Q

1st trimester screening tests?

A

1) US for nuchal translucency ( trans < 2 mm)
2) PAPP-A
3) hCG

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9
Q

2nd trimester tests

A

Triple screen = hCG, AFP, Estriol

Quad screen = add Inhibin-A

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10
Q

Pattern of 2nd trimester tests in Downs vs. Edwards

A

Downs is UP (INCREASE hCG, decrease AFP, decrease estriol, INCREASE inhibin A)

edwards (decrease hcg, AFP, estriol, inhibin A

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11
Q

Combined screen

A

1st + 2nd trimester screening done before doing any confirmatory tests = increased sensitivity, but decreased options because later in pregnancy

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12
Q

Sequential screen

A

1st tri tests

1) if positive –> invasive test
2) if negative –> 2nd tri tests

Increases number of invasive tests and thus increased fetal loss
increased options though also

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13
Q

Pre-Conception…what do you think about?

A

1) Safety (genetics, maternal age, DV, abuse)
2) Vitamins (FOLATE!)
3) Vaccines ( flu, HBV, MMRV –> want MMRV BEFORE pregnancy, because can’t give after pregnant - live vaccine)
4) Lifestyle (smoking, ETOH)
5) optimize other disease (HTN, DM, hypoT)

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14
Q

what does GPA and TPAL stand for?

A

Gravid (number of times with something in your uterus)
Para (deliver events)
Abortions

Term
Preterm
Abortions
Living

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15
Q

Initial tests in 1st trimester (around week 10)

A

1) urine preg
2) US –> confirms IUP, gestational age, if there are multiple gestations
3) serum B-HCG (confirm if too soon for US)

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16
Q

Labs at 1st trimester

A

Blood:

1) ABO type
2) Rh-Ag
3) Hgb/Hct
4) HIV, HBV, RPR
5) titers (varicella, rubella)

Urine:

1) UA + cx
2) proteinuria
3) GC/Chlamydia

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17
Q

Main things to screen for in third trimester (3)

A

1) Gestational DM
2) Alloimmunization
3) Maternal anemia

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18
Q

Gestational DM

A

DM starts AFTER 20 wks

  • Risks = increased BMI, GDB before, pre DM
  • TX with insulin
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19
Q

DX of gestational DM

A

1-hr glucose tolerance test (GTT) –> > 140 after 1 hour

3-hr GTT –> fasting > 90, 1hr > 180, 2hr > 155, 3hr >140 - must have 2/4 abnormal

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20
Q

Alloimunization (Rh Ag Status)

A
  • Rh-Ag (-) mom + Rh-Ag (+) baby + Rh-Ag (+) baby #2
  • Rh-Ag (-) mom develops Rh-Ab (+)

IF mom is Ab positive already and baby is Rh-Ag (+) –> transcranial doppler to r/o fetal anemia

IF mom is Rh-Ab negative still –> RHOGHAM at 28 weeks and within 72hrs of delivery to prevent mom from ever developing antibodies

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21
Q

normal maternal Hgb

A

Hgb > 10 or Hct > 30%

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22
Q

Treatment of UTIs in pregnancy

A

1) use amoxicillin (1st line) or Nitrofurantoin (2nd line) for asx bacteruria or cystitis
2) use CTX and admit if pyelo (cannot use TMP-SMX or cipro like usual outpatient)

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23
Q

Treatment of:

  • HYPO thyroid
  • HYPER thyroid

in pregnancy

A

HYPO thyroid –> levothyroxine (more thyroid binding globulin –> must increase dose, f/u TSH Q4wks)

HYPER thyroid –> PTU, surgery (2nd trimester)

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24
Q

what anti-epileptic drugs should be used in pregnancy

A

ideally none…if you have to use them then use Leviteracetam or lamotrigine

DO NOT use phenytoin, valproic acid, carbemazepine

TX of status –> phenobarbital

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25
Q

HTN treatment during pregnancy

A

goal <140/<80

a-methyl dopa (1st line), labetalol, hydralazine = SAFE in pregnancy

increase frequency of screening for eclampsia

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26
Q

DM before, during and after pregnancy

A 
Before = A1C < 7%, change from oral to insulin
During = increased insulin requirement, use basal-bolus based on post-pradial BS target
After = decreased insulin requirements
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27
Q

what happens if DM is out of control during pregnancy?

A

1) transposition of great vessels
2) Macrosomia –> shoulder dystocia
3) increased risk C section

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28
Q

Stages of normal labor

A

1) Stage I, latent (0-6 cm)
2) Stage I, active (6-10 cm)
3) Stage II (10 cm - fetus delivered)
4) stage III (fetus - placenta delivered)

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29
Q

Normal speed of Stage I latent and active?

A 
latent = < 20 hrs (NP) or < 14 hrs (MP)
Active = 1.2 cm/hr (NP) or 1.5 cm/hr (MP)
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30
Q

Normal speed of stage II and III

A

stage II = < 3hr (NP), < 2 hr (MP)

stage III = 30 minutes

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31
Q

what cervical changes take place

A
  • Breakage of disulfide bonds –> water

- softening, effacement, dilation, position –> 2/2 fetal head engagement (+ prostaglandins, oxytocin)

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32
Q

Fetal station

A

level of fetus from -5 (uterus) to +5 (vaginal opening) with O being in the center of the ischial spines

the more (-) = more likely to do c section

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33
Q

3 possible fetal positions?

A

1) Long cephalic (nml)
2) long breach
3) transverse

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34
Q

breach types?

A

1) Frank - hips flexed, knee extended
2) complete - hips flexed, knee flexed
3) Footling - hips extended, knees anyway

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35
Q

How to speed up latent stage I?

A

engagement of fetal head…

1) balloon
2) amniotome
3) induce with misoprostol or oxytocin (increase frequency and strength of contractions)

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36
Q

How to speed up active stage I?

A

oxytocin –> can proceed to c-section if contractions are already adequate

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37
Q

how to speed up stage II?

A

oxytocin –>

  • if baby in + fetal station (closer to vaginal opening) –> forceps, vacuum
  • if baby in - fetal station (closer to uterus) –> c-section
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38
Q

how to speed up stage III?

A

1) uterine massage
2) oxytocin
3) manual extraction

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39
Q

what are 3 possible causes of delayed stage progression?

A

3 P’s:

1) passenger
2) Pelvis
3) Power

if its a passenger or pelvis problem –> proceed to c-section

if its a power problem –> oxytocin

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40
Q

what is considered “adequate” contractions?

A

200 MV per 10 min (measure with IUPC)

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41
Q

What is considered preterm? term?

A

24-37 weeks = preterm
37-42 = term
>42 wks = post dates

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42
Q

What is considered prolonged rupture of membranes?

A

> 18 hrs

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43
Q

Rupture of Membranes

A

amniotic sac fluid released

  • spontaneous, artificially, or pathologic (usually infection)
  • can be stained with meconium, bloody, or clear
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44
Q

How do you diagnose ROM

treatment?

A

speculum exam –> see pooling
nitralazine –> blue
on a slide you see FERNING

TX:

  • term –> deliver
  • < 20 wks –> deliver
  • > 20 wks –> term (risks/benefits - infection vs. maturation of baby)
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45
Q 
Premature ROM (PROM)
-causes? (2)
A

-usually 2/2 infection, GBS

+ ROM, +term, NO contractions

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46
Q

pre-term premature ROM (pPROM)

A

-usually 2/2 infection, GBS
+ROM, NOT TERM, NO CONTRACTIONS

If > 34 weeks –> DELIVER
if < 24 weeks –> abortion

in between –> steroids

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47
Q

Endometritis/Chorioamnionitis

A

path: vaginal flora ascends
Chorio = infection of the membranes and amniotic fluid surrounding the fetus. Most common precursor to neonatal sepsis.
Endo = most common cause of post-partum fever. infection of endometrium

it is endo if baby is OUT, chorio if baby is IN
-pt is febrile and toxic looking

DX - UA, CXR, blood cx (r/o other causes)

TX gram- and anaerobes –> AMP + GENT +/- CLINDA

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48
Q

Prolonged ROM

A

vaginal flora and infection can get in (e.g. GBS)
-when > 18hrs after delivery

TX = delivery

f/u endometritis/chorioamnionitis

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49
Q

Risks of preterm delivery

A

smoking, decreaed maternal age, multiple gestations, pPROM, anatomical

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50
Q

What is preterm delivery, what do you do?

A

+ contractions AND cervical change, but NOT term

-TX –> > 34 wks = deliver
< 20 wks –> abortion
in between –> steroids, tocolytics (gives you hours/days)

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51
Q

Post Dates

A

increased risk of macrosomia, shoulder dystocia

pt > 40 wks conceptions and > 42 wks by dates

-TX depends on how sure you are on dates…if cervical is favorable positioning? Use NST, US, BAP

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52
Q

Treatment of chronic HTN in pregnancy

A

sustained HTN before 20 wks

  • use a-methyldopa, labetalol, hydralazine
  • need more frequent f/u for UA, frequent US
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53
Q

Gestational HTN

A

BP > 140/80 sustained, onset after 20 wks

no urinary or alarm sx.

f/u for progression to pre-eclampsia

54
Q

Mild pre eclampsia

A

> 140/80, sustained after 20 wks.

  • urine has > 300 ng/dL protein
  • NO alarm sx

IF > 37 wks, deliver, IF < 37 wks, wait with Q weekly f/u

55
Q

Severe pre eclampsia

A

> 160/110

urine + for 5g/dL protein
-+ ALARM SX

TX = give Mg2+ and deliver via induction

56
Q

What are the severe features in eclampsia? (7)

A 
increased Cr
HA
change in vision
decreased platelets
increased LFTs
RUQ abd pain
pulmonary edema
57
Q

Eclampsia

A

> 160/110

SEIZURES**

Give Mg2+ and deliver

58
Q

HELLP

A

Hemolysis
Elevated liver enzymes
low platelets

59
Q

Magnesium

A

used to prevent seizures in eclampsia/pre-eclampsia

  • must assess for decreased DTRs –> can progress to decreased RR if too much Mg2+
  • -> give Ca if this happens to reverse Mg2+
60
Q

Dizygotic, dichorion, diamnion

A

2 placentas, 2 sacs, 2 zygotes

babies can be different genders - 2 different fertilizations

-increased risk of preterm birth, breach birth (1 extra baby = 4 weeks early), increased post-partum hemorrhage

61
Q

Monozygotic, dichorion, diamnion

A
  • 2 placentas, 2 sacs

- 1 zygote fertilization that splits at 0-3 days

62
Q

Monozygotic, monochorion, diamnion

A
  • 1 zygote that splits at day 4-8 (blastocyst stage)
  • 1 placenta, 2 sacs
  • increased risk of twin-twin transfusion **same blood supply
63
Q

Monozygotic, monochorion, monoamnion

A

1 zygote that splits (split on day 9-12 –> non-conjoined, split on day >12 –> conjoined)

  • 1 placenta, 1 sac
  • increased of conjoined or cord entanglement
64
Q

Post partum hemorrage (PPH)

A

> 500cc for vaginal delivery
1000cc for c-section

causes: 1. uterine inversion, 2. uterine atony, 3. retained placenta, 4. vaginal lac

65
Q

Uterine inversion

A

ABSENT uterus
-uterus “births” itself –> deliver with oxytocin or traction can cause this

TX:

  • manual inversion
  • tocolytics (calm uterus down) –> oxytocin to contract it in place
66
Q

Uterine atony

A

BOGGY uterus
-tired uterus after long labor, oxytocin, tocolytics

TX:

  • massage
  • restart oxytocin (if pt was induced)
  • methergine, hemabate, or PGE drug
  • Surgery
67
Q

Retained placenta TX?

A

FIRM uterus

  • D+C –> hysterectomy
  • f/u with B-HCG to make sure all products gone (decrease risk of chorio)
68
Q

Unexplained, ongoing bleeding

A

2 large bore IVs, bolus IVF, transfuse, call surgeons, IV estrogen

Surgery –> uterine artery ligation/embolization, total abdominal hysterectomy

69
Q

DIC

A 
decreased platelets --> give platelets
decreased Hgb --> give pRBCs
increased schistocytes
decreased fibrinogen
increased INR --> give FFP
70
Q

Placenta accreta

A

placenta partially implanted into superficial myometrium instead of the decidua

  • increased risk of accreta with placenta previa
  • makes up 80% of abnormal placental implantation

-Risks = endometrial inflammation, scarring from prior C-section

71
Q

Placenta percreta

A

placental invasion through the myometrium into the uterine serosa

72
Q

Placenta increta

A

placental invasion into the uterine myometrium

73
Q

Algorithm for decreased fetal movement

A

1) NST
2) NST + VAS (vibro-acoustic stimulation)
3) BPP (biophysical profile)
4) CST (contraction stress test)

74
Q

Non-Stress Test (NST)

A

look at fetal HR, variability, and accelerations
nml HR = 110-160 with moderate variability
-want 2 or more accelerations in HR (at least 15 bpm) that last 15 seconds at a time
*2 in 20

75
Q

Biophysical profile (BPP)

A 
do if failed NST w/VAS
scoring system: each one 0-2 points = total 10
-NST
-AFI (amniotic fluid index)
-Breathing
-Movement
-Tone
76
Q

AFI (amniotic fluid index)

A

< 5 = oligohydramnios
>25 = polyhydramnios
8-25 is IDEAL

77
Q

Contraction stress test (CST)

A

can be done if contractions are present

-look for brady and late decels with decreased variability

78
Q

Early decels

A

–> head complression (benign)

decels line up with contractions

79
Q

Variable decels

A

–> cord compression (benign)

80
Q

Late decels

A

utero-placental insufficiency
**BAD

-HR devels begin after peak of contraction

81
Q

Late decels

A

utero-placental insufficiency
**BAD

-HR decels begin after peak of contraction

82
Q

Causes of 3rd trimester bleeding (5)

A

Can be split into PAINLESS (placenta, baby blood, previa) and PAINFUL (uterus, mom, NOT previa)

1) Normal
2) Placenta previa
3) Vasa previa
4) uterine rupture
5) Placental abruption

83
Q

Placenta previa

A

placenta grows over the cervical opening (os)

  • tears when the cervix dilates in 3rd trimester
  • painless bleeding in 3rd trimester

RISK: multigravid, multi-gestations

DX: US, NST/CST –> transverse lie, fetal distress –> urgent C/S

84
Q

Vasa previa

A

two accessory lobes of placenta, connected by blood vessels across os

  • painless bleed, placental blood
  • vessels tear when cervix dilates

–> DX: US, NST/CST –> fetal distress –> urgent C/S

85
Q

uterine rupture

A

happens when women have prior C/S and are receiving oxytocin
-baby can rupture into peritoneum

  • PAINFUL bleeding
  • loss of fetal station*

–> crash section

86
Q

Placental abruption

A

placenta tears off endometrial lining = COMPLETE
if bleed is contained = CONCEALED

occurs in severe HTN, cocaine, MVA

PAINFUL

DX: US, NST/CST, vitals, hgb, AMS in mom
TX: C/S

87
Q

Group B strep

A

benign colonization of mom –> for baby is really bad

  • screen women with swab and UA in wk 10 for GBS AND at week 35
  • if + then treat NOW and at delivery

-if baby gets it, they will look normal and then get SAS

88
Q

risks for GBS

A
    • GBS history
  2. prolonged ROM
  3. intrapartum fever
89
Q

Treatment of GBS

A
  • ampicillin
  • -> ceohazolin (if allergic) –> clinda or vanc if life threatening allergy

**don’t need intrapartum ppx abx is no ROM and C/S delivery

90
Q

HBV tx for baby and mom

A

C/S (avoid mixing of blood)

  • baby gets HBV vaccine and HBV IVIG
  • mom ideally vaccinated before pregnancy
91
Q

HIV tx for baby and mom

A

Mom - maximize on HAART
NNRTI = tenofavir + emcitribine OR zidovudine + lanivudine
THEN add either nevirapine or atazanavir

BABY –> give AZT at time of delivery

92
Q

Toxo

A

T. gondii, parasite found in cat feces, undercooked meat, cysts in the soil

mono-like illness in mom with acute infection (fever, malaise, lymphadenopathy)

BABY –> brain calcifications, ventriculomegaly, seizures

93
Q

Syphilis

sx?

A

T. pallidum, spirochete, STI

primary = painless chancre
secondary = targetoid lesions on palms and soles (CONTAGIOUS!)
EL/LL = + test but no sx
Tertiary = neuro sx
94
Q

Syphilis dx? tx?

A 
1 = dark field microscopy, PCN IMx1
2 = RPR --> FTP-Abs confirm, PCN IMx1
3 = CSF VDRL, IV Q4hrs 7-10 days
EL = IMx1
LL = IM Qwk x3
95
Q

Syphilis dx? tx?

A 
1 = dark field microscopy, PCN IMx1
2 = RPR --> FTP-Abs confirm, PCN IMx1
3 = CSF VDRL, IV Q4hrs 7-10 days
EL = IMx1
LL = IM Qwk x3
96
Q

Rubella

A

primary viremia is what hurts baby
Congenital rubella = blueberry muffin petechiae/purpura, cataracts, congenital heart problems, deafness

if 1st tri –> IUGR or abortion

97
Q

HSV

A

primary viremia is what causes congenital defects.
-secondary reactivation increases risk of baby getting infected

Baby –> IUGR, preterm, blindness

DX with PCR HSV from scarping of base of ulcer

98
Q

Risks of forceps and vacuum use

A

forceps –> cephalohematoma, bells palsy

vacuum –> denuding vagina

99
Q

Risks of forceps and vacuum use

A

forceps –> cephalohematoma, bells palsy

vacuum –> denuding vagina

100
Q

Grading of vaginal lacerations

A 
1 = vagina
2 = perineal body
3 = sphincter
4 = mucosa
101
Q

Cerclage

A

performed to preserve incompetent cervix

  • risk of this with PID, repeat D+C, repeat STDs
  • can cause repeat 2nd trimester loss
102
Q

Treatment of cervical CA

A

if exocervical –> LEEP

if endocervical –> cone biopsy

103
Q

If abnormal pap –> ______ –> _______

if ASCUS –> ______ –> _______

A

abnormal pap –> colposcopy –> LEEP vs. cone

ASCUS –> HPV DNA reflex testing –> Pap Q6 months and colpo if not normal

104
Q

Tx of endometrial hyperplasia

A

progesterone

105
Q

Types of ovarian cancers

A

1) Germ cell
2) Epithelial
3) Stromal

106
Q

Germ cell ovarian tumors

A

1) dysgerminoma (LDH, chemo)
2) Endometrial sinus (AFP)
3) Teratoma (not malignant, stroma ovarii)
4) Choriocarcinoma (B-HCG)

107
Q

Epithelial cell ovarian tumors

A

1) serous
2) mucinous
3) endometroid
4) Brenners

1-3 are cystadenocarcinomas

track w/CA-125, tx w/ TAH+BSO and paclitaxel

if BRCA1 or 2 –> can screen with TVUS and Ca-125 @age 35, can do ppx TAH+BSO

108
Q

Stromal cell tumors

A

1) granulosa theca cell tumors –> estrogen
2) Sertoli-leydig cell –> testosterone

present w/endocrine sx

109
Q

Complete mole

A

only paternal DNA (46XX, XY)

  • NO fetal parts
  • good fertilization, bad egg
  • sx:
    1) size-date discrepancy
    2) increased B-HCG (usually >100,000)
    3) HyperT or hyperemesis
    4) Grape-like mass protrudes through cervix

DX: TVUS shows snowstorm pattern
-HIGHER risk of chorio

110
Q

TX of complete mole

A

suction curetage

follow B-hcg for 6 months while on OCPs

111
Q

Incomplete/Partial mole

A

egg +2 sperm (69XXY, XYY)

  • good egg, bad fertilzation
  • same sx, dx, and tx as complete mole
  • LOWER risk of chorio
112
Q

Suspensory ligament of the ovary

A

contains ovarian artery and vein

–> ovarian torsion cuts off blood supply

113
Q

Uterosacral ligaments

A

Removed w/hysterectomy

-look like ureters

114
Q

Cardinal ligament

A

connect uterus to sidewall

–> cystocele, rectocele, uterine inversion occurs w/pelvic floor relaxation

115
Q

W/u of simple vs. complex cysts

A

Simple = small, unilocular, no septations, anechoic, homogenous

Complex = big, +septations, loculated, multiechoic, heterogenous

if < 3cm –> nothing
if < 10 cm –> repeat imaging (remove if it grows)
if > 10 cm –> removed w/ laparoscopy

116
Q

Complex cyst could be…(6)

A

1) tuboovarian abscess
2) teratoma
3) cancer
4) endometrioma
5) ectopic
6) torsion

117
Q

how high should B-hcg be for you to see a pregnancy on TVUS

A

1,500-2000 B-HCG –> should see IUP on TVUS

118
Q

Tuboovarian abscess

A

path: GC/CT or vaginal flora
pt: abd pain/pelvic pain
–> CMT, adnexal tenderness, uterine tenderness
+ fevere, leukocytosis
WBC of wet prep

119
Q

Tx of tuboovarian abscess

A

IV abx –> cefoxatin + doxy + mtz OR clinda + mtz

120
Q

progression of abortion

A

IUP –> threatened abortion –> inevitable –> incomplete –> complete

OPEN cervical os with inevitable and incomplete

121
Q

Causes of vaginal bleeding in a non-pregnant reproductive age woman (9)

A

Polyps
Adenomyosis
Leiomyoma
Malignancy

Coagulopathy
Ovarian dysfunction
Endometrium
Iatrogenic/IUD
Not yet classified
122
Q

Mullerian agenesis

A

nml 46(XX)
nml testosterone
nml FSH, LH

NO uterus/ovaries
nml external genitalia

123
Q

Androgen insensitivity syndrome / testicular feminization

A

-46 (XY)
-increased testosterone (resistant to testosterone)
-external female genitalia
+ TESTES
NO uterus

124
Q

Kallman’s

A

low FSH and LH, anosmia
deficiency of hypothalamic function
uterus and tubes nml, NO secondary sex characteristics

TX w/estrogen and progesterone

125
Q

Turner syndrome

A

45XO –> increased FSH and LH
STREAK ovaries
NO secondary sex characteristics
uterus present, normal external genitalia

126
Q

Causes of secondary amenorrhea

A

1) pregnancy
2) hypothyroid –> TRH inhibits ant.pit.
3) Prolactin –> prolactin inhibits GnRH
4) Meds
5) HPO axis

127
Q

Problems with anterior pituitary causing secondary amenorrhea

A

adenoma, sheehan’s syndrome, apoplexy (tumor outgrows blood supply and necroses)

128
Q

Problems with ovary causing secondary amenorrhea

A

Savage syndrome, menopause, premature ovarian failure if < 40 yrs

129
Q

Problems with endometrium causing secondary amenorrhea

A

ashermann’s, ablation

130
Q

Workup of Congenital adrenal hyperplasia

A

BL adrenal hyperplasia
17-hydroxy progesterone INCREASED in urine

TX with cortisol or fludrocortisone

OBGYN (3 decks)

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