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USMLE STEP 2 CK > OBGYN > Flashcards

OBGYN Flashcards

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USMLE® Step 1 flashcards
1
Q

Human Chrorionic Gonadotropin (hCG)

A

• Producedby syncytiotrophoblast
• Similar to LH, FSH, & TSH
• Maintains corpus luteum (of progesterone until the placenta can take over
maintenance of the pregnancy.)

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2
Q

Human Placental Lactogen (hPL)

A
  • Producedby syncytiotrophoblast
  • Similar to HGH, prolactin
  • Decreases insulin sensitivity
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3
Q

Progesterone

A
  • Produced by corpus luteum - after the ovulation
  • Prepares endometrium for implantation
  • Decreasedmyometrial contractility
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4
Q

Estradiol
Estriol
Estrone

A
  • estradiol during the nonpregnant reproductive years
  • estriol during pregnancy
  • estrone during menopause
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5
Q

PHYSIOLOGIC CHANGES IN PREGNANCY

Endocrine

A 
Skin
Cardiovascular
Hematologic
Gastrointestinal
Pulmonary 
Renal 
Endocrine
- pituary size increase + risk of Sheehan syndrome from postpartum hypotension
- increase production of cortisol
- thyroid size increase, + TBG --> + total T3 T4 but free T3 and T4 levels remain unchanged
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6
Q

PHYSIOLOGIC CHANGES IN PREGNANCY

Renal

A 
Skin
Cardiovascular
Hematologic
Gastrointestinal
Pulmonary 
Endocrine
Renal 
- ureteral diameter increases to progesterone 
- GFR increases
- urine glucose increases
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7
Q

PHYSIOLOGIC CHANGES IN PREGNANCY

Pulmonary

A 
Skin
Cardiovascular
Hematologic
Gastrointestinal
Endocrine
Renal
Pulmonary 
- VT increases; ONLY LUNG VOLUME that DOES NOT DECREASE
- RV decreases
- Increase in VT produces a resp alkalosis with a decrease in PCo2
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8
Q

PHYSIOLOGIC CHANGES IN PREGNANCY

Gastrointestinal

A 
Skin
Cardiovascular
Hematologic
Endocrine
Renal
Pulmonary 
Gastrointestinal
Stomach
- motility decrease and emptying time increase from the progesterone effect
\+ risk aspiration
Large bowel
- motility decrease and transit time increase + constipation
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9
Q

PHYSIOLOGIC CHANGES IN PREGNANCY

Hematologic

A 
Skin
Cardiovascular
Endocrine
Renal
Pulmonary 
Gastrointestinal
Hematologic
- RBC increases, + oxygen-carrying capacity, + plasma volume and dilutional effect, not anemia
- WBC increases
- ESR increases 
- Coagulation factor increases
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10
Q

PHYSIOLOGIC CHANGES IN PREGNANCY

Cardiologic

A 
Skin
Endocrine
Renal
Pulmonary 
Gastrointestinal
Hematologic
Cardiovascular
- Systolic DECREASE - 
- Diastolic DECREASE - -
- Central venous UNCHANGED
- Venous femoral INCREASE
- Vascular resistance DECREASE
- Arterial blood pressure: never elevalated in pregancy 
- CO increase; SV increase by the end of the first trimester; CO dependant on the maternal position (lowest supine, highest left lateral)
- Systolic murmur NORMAL (increase CO); Diastolic ALWAYS pathologic
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11
Q

PHYSIOLOGIC CHANGES IN PREGNANCY

Skin

A

Skin
Striae gravidarum—“Stretch marks” that develop in genetically predisposed women on the abdomen and buttocks.

Spider angiomata and palmer erythema—From increased skin vascularity.

Chadwick sign—Bluish or purplish discoloration of the vagina and cervix as a result of
increased vascularity.

Linea nigra—Increased pigmentation of the lower abdominal midline from the pubis to the umbilicus.

Chloasma—Blotchy pigmentation of the nose and face.

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12
Q

Fetal Circulation Shunts

A
  • Ductus venosus(UA→IVC)
  • Foramen ovale (RA → LA)
  • Ductus arteriosus (PA → DA)
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13
Q

Hormones for lactation

A

DEVELOPEMENT
• Estrogen, released from the ovarian follicle, promotes the growth ducts.
• Progesterone, released from the corpus luteum, stimulates the development of milk-
producing alveolar cells.
• Prolactin, released from the anterior pituitary gland, stimulates milk PRODUCTION

RELEASE
• Oxytocin, released from the posterior pituitary in response to suckling, causes milk ejection from the lactating breast.

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14
Q

Colostrum

A

more protein and less fat than subsequent milk, and contains IgA antibodies that impart some passive immunity to the infant.
Most of the time it takes 1 to 3 days after delivery for milk production to reach appreciable levels.

  • expulsion of the placenta initiates the milk production and drop of estrogen and progesterone; estrogen antagonizes positive effect of milk production
  • physical stimulation + oxytocin + production
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15
Q

Post-conception Week 1-8

Trilaminar layers

A

Post-conception Week 1
• Starts at conception
• Ends with implantation
• Yieldsmorula→blastula

Post-Conception Week 2
• Starts with implantation
• Ends with 2-layer embryo
• Yields bi-laminar germ disk

Post-Conception Week 3
• Starts with 2-layer embryo
• Ends with 3-layer embryo
• Yields tri-laminar germ disk; ectoderm; mesoderm and endoderm

Post-Conception Week 4-8
• 3 germ layers differentiating
• Greatest risk of malformations
• Folic acid prevents NTD

  • Ectoderm—central and peripheral nervous systems; sensory organs of seeing and hearing; integument layers (skin, hair, and nails).
  • Mesoderm—muscles, cartilage, cardiovascular system, urogenital system.
  • Endoderm—lining of the gastrointestinal and respiratory tracts.
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16
Q

Paramesonephric (Müllerian) Duct

A

the primordium of the female internal repro- ductive system. No hormonal stimulation is required.

In males the Y chromosome induces gonadal secretion of müllerian inhibitory factor (MIF), which causes the müllerian duct to involute.

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17
Q

Female External Genitalia

A

No hormonal stimulation is needed for differentiation of the external genitalia into labia majora, labia minora, clitoris, and distal vagina.

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18
Q

Mesonephric (Wolffian) Duct

A

Testosterone stimulation is required for development to continue to form the vas deferens, seminal vesicles, epididymis, and efferent ducts.

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19
Q

Male External Genitalia

A

Dihydrotestosterone (DHT) stimulation is needed

Stertoli Cell –> Anti-Mullerian Hormone –> Inhibit Mullerian develp

Leydig cell –> testosterone –>maintains wolffian duct develp

Testoterone –> (5a-reductase)–> Dihydro-testosterone –> virilizes urogenital sinus, external gentila

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20
Q

The period of greatest teratogenic risk

A

Postconception weeks 3–8 because formation of the 3 germ layers to completion of organogenesis.

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21
Q

Fetal alcohol syndrome

A

IUGR, midfacial hypoplasia, developmental delay, short palpebral fissures, long philtrum, multiple joint anomalies, cardiac defects.

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22
Q

Isotretinoin (Accutane) pregnancy

A

Congenital deafness, microtia, CNS defects, congenital heart defects.

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23
Q

Lithium pregnancy

A

Ebstein’s anomaly (right heart defect).

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24
Q

Valproic acid pregnancy

A

Neural tube defects (spina bifida), cleft lip, renal defects.

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25
Q

Warfarin (Coumadin)

A

Chondrodysplasia (stippled epiphysis), microcephaly, mental retarda-
tion, optic atrophy.

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26
Q

Turner Syndrome

A 
45, X
gonadal dysgenesis or monosomy X
• Primary amenorrhea
• Web neck
• Streak gonads
Coartaction of aorta

nuchal skin-fold thickening

27
Q

Klinefelter Syndrome

A 
47, XXY
• Testicular atrophy
• Gynecomastia
• Azoospermia
tall stature, learning disorders, low IQ
28
Q

Down Syndrome

A 
Trisomy 21
• Short stature
• Mental retardation
• Endocardial cushion cardiac defects
duodenal atresia

oblique orbital fissures, flat nasal bridge, small ears, nystagmus, and protruding tongue

29
Q

Autosomal Recessive

A

• Transmitted by both sexes
• Often skips generations
• Male and female carriers
CF, thalassemia, deafness, sickle cell disease, CAH, wilson disease, Tay-Sach disease, albinism

30
Q

X-Linked Recessive

A

• No male–male transmission
• Expressed only in males
• Female carriers
- Hemophilia A, diabetes insipidus, hydrocephalus, G-6-PD, duchene, color blindness

31
Q

Methods of Induced Abortion

A

First trimester

  • Surgical: D&C
  • Medical: Mifepristone: progesterone antagonist

Second trimester higher rate of complication

  • Surgical: D&E
  • Induction of labor contractions
32
Q

Missed abortion

A

Sonogram finding of a nonviable pregnancy without vaginal bleeding, uterine cramping, or cervical dilation.

Management:

  • Scheduled suction D&C
  • conservative management awaiting a spontaneous completed abortion, or - induce contractions with misoprostol.
33
Q

Threatened abortion

A

viable pregnancy with vaginal bleeding but no cervical dilation. Half of these pregnancies will continue to term successfully.

Management: Often the cause is implantation bleeding.

  • Observation.
  • No intervention is generally indicated or effective
34
Q

Inevitable abortion

A

Vaginal bleeding and uterine cramping leading to cervical dilation, but no POC has yet been passed.

Management:
Emergency suction D&C if bleeding is heavy to prevent further blood loss and anemia.
Otherwise conservative management awaiting a spontaneous completed abortion or induce contractions with misoprostol.

35
Q

Incomplete abortion

A

Vaginal bleeding and uterine cramping leading to cervical dilation, with some, but not all, POC having been passed.

Management: Emergency suction D&C if bleeding is heavy to pre- vent further blood loss and anemia. Otherwise conservative management awaiting a sponta- neous completed abortion or induce contractions with misoprostol.

36
Q

Completed abortion

A

Vaginal bleeding and uterine cramping have led to all POC being passed. This is confirmed by a sonogram showing no intrauterine contents or debris

Management: Conservative if an intrauterine pregnancy had been previously confirmed. Otherwise, serial b-human chorionic gonadotropin (b-hCG) titers should be obtained weekly until negative to ensure an ectopic pregnancy has not been missed.

37
Q

Fetal demise

A

Significance
- Disseminated intravascular coagulation (DIC) is the most serious consequence with prolonged fetal demise (>2 weeks) resulting from release of tissue thromboplastin from deteriorating fetal organs.

Presentation

  • Before 20w; usually uterine fondus less than date
  • After 20w; absence of fetal movements
38
Q

A 28-year-old patient visits the emergency department complaining of unilateral left-sided abdominal pain and vaginal spotting of 3 days’ duration. Her last menstrual period was 8 weeks ago, and before this episode she had menses every 28 days. Her only previous pregnancy was an uncomplicated term spontaneous vaginal delivery. She had used intrauterine contraception for 3 years in the past. On pelvic examination the uterus is slightly enlarged and there is left adnexal tenderness but no palpable mass. A quantitative serum b-hCG value is 2,600 mIU.

A

Ectopic Pregnancy
• Secondary amenorrhea
• Unilateral abdominal/pelvic pain
• Vaginal bleeding

  • outside the uterine cavity; MC location is distal ampulla
  • risk factors: PID, infectious IUD, postsurgical (tubal ligation), congenital (DES exposure)
  • if patient had 1 ectopic, the incidence becomes 15%
  • signs: unilateral, cervical tenderness
    if ruptured: peritoneal irritation and hypovolemia
  • investigation: b-HCG + no intrauterine pregnancy
  • Ruptured: surgical emergency; salpingectomy + B-HCG titers + RhoGam
  • Unruptured: methorexate (folate antagonist) + series of B-HcG and Rh- female give RhoGAM
    or surgical: salpingostomy
39
Q

A 28-year-old multigravida at 33 weeks’ gestation comes to the office stating she has not felt her baby move for 24 hours. A previous 18-week sonogram showed a single fetus with grossly normal anatomy. You are unable to find fetal heart tones by auscultation with a Doppler stethoscope.

A

Fetal Demise

40
Q

Unsafe immunizations

A 
live attenuated organisms: 
• Measles
• Mumps
• Polio
• Rubella
• Yellow fever • Varicella
41
Q

FIRST TRIMESTER LABORATORY TESTS

A 
CBC
Rubella IgG Antibody
Rubella IgG Antibody
Type, Rh, and Antibody Screening
Urine Screening: Screening for asymptomatic bacteriuria (ASB) is essential. 
HIV Screening
\+/- STD Screening

Direct Coombs test
The patient’s blood type and Rh is determined with the direct Coombs test. If the patient is Rh negative, she is at risk for anti-D isoimmunization.

42
Q

SECOND TRIMESTER LABORATORY TESTS

A

Alpha-Fetoprotein:
+ in open neural tube defect [NTD] and ventral wall defects, twin, teratoma, placental bleeding; if high make sure the dating is accurate
- trisomy 21

Trisomy screening
MS-AFP, but also hCG, estriol, and inhibin-A

43
Q

THIRD-TRIMESTER LABORATORY TESTS

A

1-h 50-g oral glucose tolerance test (OGTT )

  • 24 and 28 weeks’ gestation
  • no fasting needed

CBC

GBS; 30 weeks

44
Q

LATE PREGNANCY BLEEDING

A

after 20 weeks’ gestation
NEVER DO DIGITAL EXAM UNTIL CONFIRMED NO PLACENTA PREVIA

DDX
Placental Abruption 
Placenta Previa
Vasa Previa
Uterine Rupture
Cervical Insufficiency
Vaginal or Cervical Etiologies 
Lacerations/trauma
Cervical friability
Cancers
45
Q

Placental Abruption

A

Placental separation from its implantation site before delivery

Risk factors: Prior abruption, Cocaine Use, Hypertension, Preeclampsia, Smoking, PPROM, Thrombophilias, Multiple gestation, Polyhydramnios, Advanced maternal age (>35 years)
Trauma

Clinical Diagnosis
Vaginal bleeding - 78%
Abdominal pain - 66%
Fetal Distress - 60%

Management:
Depends on the degree of abruption.

No fetal distress/no evidence of hemorrhage:

  • Consider other factors: GA, Celestone, etc.
  • Close monitoring warranted.

Hemorrhagic Shock:
ABCs
Emergency c-section
Intensive resuscitation with blood and crystalloids.

46
Q

Placenta Previa

A

Def: Placenta overlying cervical os.

Risk factors: Advanced maternal age, Multiparity (>5), Prior Ceasarean Section, Higher order pregnancy, Smoking

Diagnosis: Transvaginal or Transabdominal U/S

47
Q

Vasa Previa

A

Umbilical vessels, unsupported by either the umbilical cord or placental tissue, Velamentous cord insertion a prerequisite!

Risk factors: Placenta previa

Clinical diagnosis

Hospitalization at 30-32 weeks GA
Administration of Celestone
Serial TV U/S

48
Q

A 32-year-old multigravida at 31 weeks’ gestation is admitted to the birthing unit after a motor-vehicle accident. She complains of sudden onset of moderate vaginal bleeding for the past hour. She has intense, constant uterine pain
and frequent contractions. Fetal heart tones are regular at 145 beats/min. On inspection her perineum is grossly bloody.

A

Placental Abruption

Abruptio Placenta
• Late trimester painful
bleeding
• Normal placental implantation
• Disseminatedintravascular coagulopathy (DIC)

Severe abruption, symptoms are usually abrupt with a continuous knifelike uterine pain. Greater than 50% of placental separation occurs. Fetal monitor shows severe late decelerations, bradycardia, or even fetal death. Severe disseminated intra- vascular coagulation (DIC) may occur.

49
Q

A 34-year-old multigravida at 31 weeks’ gestation comes to the birthing unit stating she woke up in the middle of the night in a pool of blood. She denies pain or uterine contractions. Examination of the uterus shows the fetus to be in transverse lie. Fetal heart tones are regular at 145 beats/min. On inspection her perineum is grossly bloody.

A

PLACENTA PREVIA
• Late trimester bleeding
• Lower segment placental implantation
• No pain

placenta is implanted in the lower uterine segment.

most dangerous location: TOTAL

50
Q

Profound hypotension in pregnant women

A

Profound hypotension can cause anterior pituitary necrosis (Sheehan syndrome) or acute tubular necrosis.

51
Q

Abnormal Placental Invasion

A
  • Accreta: deeper layers decidua basalis; MOST COMMON
  • Increta: myometrium not complete
  • Percreta: uterine serosa or bladder
52
Q

A 21-year-old primigravida at 38 weeks’ gestation is admitted to the birthing unit at 6-cm dilation with contractions occurring every 3 min. Amniotomy (artificial rupture of membranes) is performed, resulting in sudden onset of bright red vaginal bleeding. The electronic fetal monitor tracing, which had showed a baseline fetal heart rate (FHR) of 135 beats/min with accelerations, now shows a bradycardia at 70 beats/min. The mother’s vital signs are stable with normal blood pressure and pulse.

A

VASA PREVIA

  • Amniotomy—AROM
  • Painless vaginal bleeding
  • Fetal bradycardia

Vasa previa is a condition which arises when fetal blood vessels implant into the placenta in a way that covers the internal os of the uterus.

53
Q

A 27-year-old G2 P1 woman comes to the maternity unit for evaluation for regular uterine contractions at 34 weeks’ gestation. Her previous delivery was an emergency cesarean section at 32 weeks because of hemorrhage from placenta previa. A classical uterine incision was used because of lower uterine segment varicosities. Pelvic exam shows the cervix to be closed and long. As she is being evaluated, she experiences sudden abdominal pain, profuse vaginal bleeding, and fetal bradycardia. Uterine contractions cannot be detected. The fetal head, which was at –1 station, now is floating.

A

UTERINE RUPTURE

54
Q

A 20-year-old woman G2 P1 is admitted to the birthing unit at 35 weeks’ gestation in active labor at 6-cm dilation. Her prenatal course was unremarkable with the exception of a positive first-trimester urine culture for GBS. Her first baby was hospitalized for 10 days after delivery for GBS pneumonia.

A

GBS Neonatal Sepsis
• Newborn sepsis
• Within hours of birth
• Bilateral diffuse pneumonia

Early onset: pneumonia and sepsis
Late onset: meningitis

Thirty percent of women have asymptomatic vaginal colonization with GBS; 35–37 weeks gestational age

55
Q

A 26-year-old primigravida was admitted to the birthing unit at 39 weeks’ gestation in active labor at 6-cm dilation. During her second trimester she experienced a mononucleosis-like syndrome. Uterine fundal growth lagged behind that expected on the basis of a first-trimester sonogram. Serial sonograms showed symmetrical intrauterine growth retardation (IUGR). She delivered
a 2,250-g male neonate who was diagnosed with microcephaly, intracranial calcifications, and chorioretinitis.

A

TOXOPLASMOSIS
• Chorioretinitis
• Intracranial calcifications
• Symmetrical IUGR

First-trimester infection risk is low (15%), but infections are most serious, even lethal.

Third-trimester infection risk is high (50%), but infections are mostly asymptomatic.

Prevention. Avoid infected cat feces, raw goat milk, and undercooked meat.

56
Q

A 29-year-old woman (G2 P1) is at 34 weeks’ gestation. She complains of uterine
contractions every 5 min. During the last few days she has developed diffuse
pruritic vesicles on her neck that appear to be also developing on her chest and breasts. She has a fever and complains of malaise.

A

VARICELLA (VZV); respiratory droplets

Prevention. Administer VZIG (varicella zoster immune globulin) to a susceptible gravida within 96 h of exposure. Live-attenuated varicella virus (Varivax III) can be administered to nonpregnant or postpartum to varicella IgG-antibody–negative women.

57
Q

An 18-year-old primigravida is at 30 weeks’ gestation and is employed in a childcare center. One of the children had a rash that was diagnosed as rubella. The patient’s rubella IgG titer is negative. She is concerned about the possibility of her fetus getting infected with rubella.

A 
Rubella: 
• Congenital deafness
• Congenital cataracts
• Congenital heart disease
“blueberry muffin” rash

Prevention.
All pregnant women should undergo rubella IgG antibody screening. Rubella-susceptible women should avoid known rubella cases, then receive active immunization after delivery. Because rubella vaccine is made using a live attenuated virus, pregnancy should be avoided for 1 month after immunization.

58
Q

A 31-year-old neonatal intensive care unit nurse has just undergone an uncomplicated term spontaneous vaginal delivery of a 2,300-g female neonate with a diffuse petechial rash. At 12 weeks’ gestation she experienced a flulike syndrome with right upper quadrant pain. Obstetric sonograms showed fetal growth was only at the fifth percentile.

A

Cytomegalovirus (CMV); DNA herpes virus that is spread by infected body secretions
• Most common congenital viral syndrome
• Most common cause of deafness in children
• Neonatalthrombocytopenia and petechiae

Prevention. Follow universal precautions with all body fluids. Avoid transfusion with CMV- positive blood.

Treatment. Antiviral therapy with ganciclovir.

59
Q

A 21-year-old multipara was admitted to the birthing unit at 39 weeks’ gestation in active labor at 6-cm dilation. The bag of water is intact. She has a history of genital herpes preceeding the pregnancy. Her last outbreak was 8 weeks ago. She now complains of pain and pruritis. On examination she had localized, painful, ulcerative lesions on her right vaginal wall.

A

HERPES SIMPLEX VIRUS (HSV)

Prevention. A cesarean section should be performed in the presence of genital HSV lesions at the time of labor. If membranes have been ruptured >8–12 h, the virus may already have infected the fetus and cesarean delivery would be of no value.

Treatment. Acyclovir.

60
Q

A 21-year-old primigravida at 15 weeks’ gestation is seen for a routine prenatal visit. At her last visit 4 weeks ago, her uterus was appropriate for size and dates. Today, her uterine fundus is palpable at the umbilicus.

A

Multiple Gestation

Complications for all twin pregnancies include nutritional anemias (iron and folate), pre- eclampsia, preterm labor (50%), malpresentation (50%), cesarean delivery (50%), and post- partum hemorrhage.

61
Q

A 22-year-old primigravida at 33 weeks’ gestation comes to the birthing unit stating that 2 h ago she had a gush of fluid from her vagina. She denies vaginal bleeding or uterine contractions. Her perineum appears moist to gross inspection.

A

Ruptured Membranes
• Posterior fornix pooling
• Fluid is Nitrazine (phenaphthazine) (+)
• Glass slide drying: fern (+)

Risk Factors. Ascending infection from the lower genital tract is the most common risk fac- tor for PROM. Other risk factors are local membrane defects and cigarette smoking.

Chorioamnionitis is diagnosed clinically with all the following criteria needed:
• Maternal fever and uterine tenderness in the presence of confirmed PROM in the absence of a URI or UTI

62
Q

What are the 5 components of the Bishop’s Score?

A

Cervical dilation, cervical effacement, fetal station, cervical position, cervical consistency

63
Q

What does a higher Bishop’s Score indicate?

A

the more likely the patient will have a successful vaginal delivery

lower- more likely to have C-Section

64
Q

A 21-year-old primigravida without severe features is seen in the outpatient prenatal clinic for routine visit. She is at 32 weeks’ gestation, confirmed by first trimester sonogram. She denies headache, epigastric pain, or visual disturbances. She has gained 10 pounds since her last visit 2 weeks ago. On examination her BP is 155/95, and remains unchanged on repeat check in 15 min. She has 2+ pedal edema, and her fingers appear swollen. A spot urine dipstick shows 2+ protein.

A

Preeclampsia
• Pregnancy >20 wk
• Sustained HTN (>140/90 mm Hg)
• Proteinuria (≥300 mg/24 h)

Preeclampsia is found 8 times more frequently in primiparas. Other risk factors are multiple gestation, hydatidiform mole, diabetes mellitus, age extremes, chronic hypertension, and chronic renal disease.

HELP
Hemolysis
Elevated 
Liver enzymes
Low
Platelets

Labetalol safe in pregnancy

USMLE STEP 2 CK (1 decks)

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