Ob & Gyn Form 4 by Omar Peter

1. A. Patient autonomy: The right of patients to make decisions about their medical care
without their health care provider trying to influence the decision. Patient
autonomy does allow for health care providers to educate the patient but does not
allow the health care provider to make the decision for the patient.
Patient’s capacity: means the patient has the mental capacity to make decisions
regarding his or her medical care. A patient lacks capacity might be declared
“incompetent” by the legal/judicial system, to be judged competent the patient must”
(1) Not be diagnosed as presently psychotic or intoxicated
(2) Have an understanding of his or her medical situation
(3) Must be capable of making decisions that are in agreement with his or her history of
values
Competent patient can decide to accept or refuse or discuss medical care options
according to his or her religious views.
B. do not shift patients to others in USMLE
C. Patient is competent and has the right to decide no guardian needed
D. E. Can’t perform C/S against patient’s will

2. B. Ultrasonography to make sure it is not malpresentation (breech or transverse..) , if

you see on US cephalic presentation then you can augment with Oxytocin (C), if breech
presentation it depends the type and patient’s wishes, if you see other presentations like
transverse then (E) Caesarian section. (A) is not done nowadays during labor, and (D)
amniotomy in this case may carry the risk of cord prolapsed and will complicate C/S if
you have transverse lie.
3. E. Hysterectomy, the general treatment of endometrial adenocarcinoma is as follow:
a. Total abdominal hysterectomy with bilateral salpingo-oophorectomy (TAH-BSO)
and lymph node sampling
b. Women who have cancer limited to the endometrial lining and who desire to
maintain fertility can be treated temporarily with progestins to limit growth but
should have TAH-BSO following childbearing years.
c. Surgical debulking should be performed for large tumors unable to be completely
resected.
d. Radiation therapy an evaluation of the post op pathology report will calssify patients
into poor or good prognosis category, patients with poor prognosis should be considered
for radiation therapy : -mets to LN - >50% of myometrial involvement - + surgical margin
– poorly differentiated
e. Chemotherapy (in place of radiation) used for any cases with spread beyond the
uterus
f. Hormone therapy (e.g., progesterone, tamoxifen) may be beneficial for advanced
tumors not cured by surgery and radiation.

4. G. Uterine Synechiae. (Asherman syndrome) results from intrauterine adhesions due

to surgery or infections, the other causes either cause infertility with no amenorrhea
 which does not fit here and if they cause amenorrhea this one is the most reasonable
given the curettage and the endometritis history.
5.C Placenta Previa risk factors Up to date: Previous placenta previa, previous cesarean
deliveries, and multiple gestation are major risk factors for placenta previa, the
whole list:
Previous placenta previa
Previous cesarean delivery
Multiple gestation
Multiparity
Advanced maternal age
Infertility treatment
Previous abortion Maternal cocaine use
Previous intrauterine surgical procedure Male fetus
Maternal smoking Non-white race

6. D. UTD states that Arrest of labor is diagnosed at cervical dilation ?6 cm in a patient with ruptured membranes and
No cervical change for 4 hours despite adequate contractions (200 MVUs). Here ihe contractions are adequate
and the arrest lasted 4 hours although the the cervix is dilated to 5 cm only. UTD mentioned on the other hand that
"at 6 cm dilation, nearly all women should be in active labor, so this means that in some women it may start
earlier specially when we find in this case that there are molded cervix and caput succedaneum.
Also protraction means that cervical dilation is slower than normal range but not that the dilation is completely arrested though.
Contraversial Q but answer is confirmed

7. D. Pulmonary embolus (pregnancy is a hypercoagulable state + tachycardia and

tachypnea + left sided pleuritic chest pain + ABG values)

8. E. Vaginal foreign body (a very similar Uworld q exists with those signs and symptoms
are mostly goes with vaginal FB due to tissues or similar things used improperly by kids)

9. A. BMI The burden of suffering associated with osteoporosis is related to the increased
incidence of fractures in individuals with low bone mass and microarchitectural
deterioration. Fragility fractures are defined as fractures that occur following a fall from
standing height or less or with no trauma. Although the greatest relative risk of fracture is
in individuals with osteoporosis, the absolute number of fractures in those with BMD T-
scores in the low bone mass (osteopenia) range is the same or greater than in those
with T-scores in the osteoporosis range.
ASSESSMENT OF FRACTURE RISK — Screening for osteoporosis involves fracture
risk assessment and measurement of BMD. Most fractures occur in women and men
who do not have osteoporosis by DXA criteria. Individuals with osteoporosis are at the
highest relative risk of fracture, but there are more fractures in patients with low bone
mass or osteopenia (T-score between -1.0 and -2.5) because there are so many more
patients in this category. Therefore, assessment of risk factors that are independent of
BMD(Bone Mineral Density) is important for fracture prediction. Validated risk factors
that are independent of BMD include the following:
 Advanced age
Previous fracture
Long-term glucocorticoid therapy
Low body weight (less than 58 kg [127 lb])
Family history of hip fracture
Cigarette smoking
Excess alcohol intake
The most robust non-BMD risk factors are age and previous low trauma fracture.
B. Family History of Fracture: will be important in this question if was non traumatic D.
Tamoxifen increases mean bone mineral density but not sure if has any effect on
fracture reduction or not. E. current Tobacco is a risk factor but in this question it seems
to be not of big significance.(2 cigarettes weekly only)

10. E. Arrange for immediate psychiatric evaluation is the answer, which might lead to
prescribing Antipsychotics, Anti depressants and not leaving the baby with the mother(
most are bipolar disorders and to a lesser extent brief psychotic disorder.

11. B. Fetal Growth Restriction The main impact on the fetus is undernutrition as a result
of utero-placental vascular insufficiency, which leads to growth retardation.

12. E. Normal Labor

13. A. Detrusor Hyperreflexia

Detrusor hyperreflexia, the most common urodynamic abnormality in MS, is now referred
to as 'neurogenic detrusor overactivity'
Classifying type of incontinence from symptoms — Little is known about how factors
such as age, race/ethnicity, and comorbidity affect the reliability and validity of specific
urinary symptoms in predicting the type of incontinence. However, several generalization
can be made:
Urgency symptoms (eg "Do you experience such a strong and sudden urge to void that
you leak before reaching the toilet?") are sensitive and specific for the diagnosis of urge
incontinence (positive likelihood ratio (LR) 4.2, 95% CI 2.3-7.6; negative LR 0.48, 0.36-
0.62) [ 30 ]. A report of such symptoms is also a reliable diagnostic tool, with
approximately a 90 percent agreement between two interviews [ 31 ].
Leakage with stress maneuvers (coughing, laughing, bending over, running, changing
position) has the same reliability as urgency symptoms and is highly sensitive but has
lower specificity [ 30 ]. "Stress" leakage can occur with detrusor overactivity, DHIC, and
incomplete bladder emptying.
Frequency, nocturia, slow urine stream, hesitancy, interrupted voiding, straining, and
terminal dribbling are commonly associated with urinary incontinence. These symptoms
lack diagnostic specificity and may occur with detrusor overactivity, DHIC, outlet
obstruction, detrusor underactivity, fluid intake, medications, and many medical
conditions.
 Nocturia may be related to nocturnal polyuria (eg, from late evening beverages, pedal
edema, congestive heart failure, or sleep apnea), sleep disturbance (eg, from
depression, pain, or medication), or from the lower urinary tract (detrusor overactivity,
eg, benign prostatic enlargement).

Postvoid residual volume — Postvoid residual (PVR) testing, by catheterization or

ultrasound, is recommended in current guidelines for evaluation of incontinence.
However, high quality evidence from randomized trials is not available to support this
recommendationPostvoid residual volume — Postvoid residual (PVR) testing, by
catheterization or ultrasound, is recommended in current guidelines for evaluation of
incontinence. However, high quality evidence from randomized trials is not available
to support this recommendation

14. F. Vesicovaginal fistula

15. F. Intraductal papillama
Pathologic (suspicious) nipple discharge — Secretory production of fluids other than
milk may be due to a pathological process in the breast. The discharge is usually
unilateral and localized to a single duct, persistent, and spontaneous. It can be serous
(clear or yellow), sanguinous (bloody), or serosanguineous (blood-tinged).
The most common cause of pathologic nipple discharge is a papilloma A papilloma is a
papillary tumor growing from the lining of the breast duct. The discharge associated with
a papilloma can be clear or grossly bloody. Solitary papillomas can harbor areas of
atypia or ductal carcinoma in situ (DCIS).
The standard recommendation for management of papillomas is that they be excised
whenever they are diagnosed by core needle biopsy, although there is some debate in
the literature . The remaining cases are caused by ductal ectasia or other benign
changes .
Malignancy is found in 5 to 15 percent of cases of pathologic nipple discharge. The most
common malignancy associated with nipple discharge in the absence of other findings is
DCIS. Age is predictive of the risk of cancer in women with nipple discharge. In one
series of women with isolated nipple discharge, malignancy was present in 3 percent of
those <40 years of age, 10 percent of those 40 to 60 years of age, and 32 percent of
those over 60
16. A. Carpal Tunnel Syndrome
17. E. IUD
Effectiveness — The effectiveness of a contraceptive method is expressed as both
the theoretical (perfect use) efficacy and the actual (typical use) effectiveness. actual
effectiveness is usually lower due to inconsistent or incorrect use. Actual
effectiveness is also influenced by frequency of intercourse, age, and regularity of
menstrual cycles, as pregnancy is less likely in women who are older, have
infrequent sexual intercourse, and have irregular menstrual cycles.
In practice, contraceptive methods can be divided into three categories based upon their
theoretical and actual effectiveness:
Most effective : Long-acting reversible contraception (intrauterine contraception,
contraceptive implants) and sterilization are associated with a low pregnancy rate
 regardless of the population studied, as the rate is minimally influenced by adherence.
Women should be encouraged to first consider a method from this tier of options.
Effective : Injectable contraceptives are the most effective in this tier of choices. OCs,
the transdermal contraceptive system, and the vaginal ring are also associated with a
very low pregnancy rate if they are taken consistently and correctly, but actual
pregnancy rates are substantially higher because of inconsistent/incorrect use.
Least effective : Other methods of contraception, including diaphragm/cervical caps,
condoms, spermicides, withdrawal, and periodic abstinence are associated with actual
pregnancy rates that are much higher than perfect use rates.

18. D. Sustained uterine contraction exaggerated by oxytocin can decrease the blood flow to the fetus,
thus causing late decelerations.

19. B. Down Syndrome

20. A. Use Lubricant

In the postpartum period, estrogen levels decline secondary to the loss of placental estrogen.
Women who breastfeed have high levels of prolactin that exert an antagonistic action on estrogen
production. can cause urogenital atrophy, Symptomatic hypoestrogenic vulvovaginal changes are
often referred to as atrophic vaginitis and typically present as vaginal dryness, itching, burning,
irritation, and dyspareunia. Hypoestrogenemia may also cause urinary symptoms such as
dysuria, urgency, and frequency
The management of atrophic vaginitis may include lubricant, estrogen replacement, and botanical
therapies, as well as education.

21. E. VZ IG therapy
The onset of maternal varicella from 5 days before to 2 days after delivery may result in
overwhelming infection of the neonate and a fatality rate as high as 30%. This severe disease is
believed to result from fetal exposure to varicella virus without the benefit of passive maternal
antibody. Infants born to mothers with onset of maternal varicella 5 days or more prior to
delivery usually have a benign course, presumably due to passive transfer of maternal antibody
across the placenta, so babies in this condition are given Varicella Zoster immunoglobulin

22. C. Condylomata Acuminata

23. A. Amenorrhea
Risk of overzealous sharp curettage is Asherman syndrome

24. A. Atelectasis

25. B. Increased cervical cell vulnerability to infections

The endocervical canal functions as a barrier protecting the normally sterile upper
genital tract from the organisms of the dynamic vaginal ecosystem. Disturbance of
this barrier provides vaginal bacteria with access to the upper genital organs via
canalicular routes, infecting the endometrium, then endosalpinx, ovarian cortex,
pelvic peritoneum, and their underlying stroma. This is the clinical entity of PID.
A. Immature immune system? I don’t see why would this be the answer, if the
question is referring to MAC complex deficiency then this will probably makes sense
but it is a defect rather than immaturity of the system. ….???
C. Increased concentration of progesterone? NO IDEA
D. Latex hypersensitivity will probably cause problems with condoms but the q does
not say if they stopped using condoms because of problems.
 E. Menarche before 14 (Early age of sexual intercourse is a risk factor for PID in
general)

26. A. Chlamydia trachomatis inf.

B. Endometrial polyp rare in this age, predictable vaginal bleeding with intermenstrual
bleeding, no pain
C. Levonorgestrel induced endometrial atrophy (Levonorgestrel could be part of
combined OCP or as an emergency pill by itself, the side effects of this medication could
be quite similar to the presentation here: pain, bleeding, cramps… but no cervical or
uterine tenderness??)

27. D. Pedunculated submucous leiomyoma uteri

This can't be incomplete abortion as the LMP was 2.5 weeks ago, so if pregnancy occured, the fetus GA would have been less than a week.

28. D. Vaginal Metronidazole gel

PATHOGENESIS AND MICROBIOLOGY — Bacterial vaginosis (BV) represents a
complex change in the vaginal flora characterized by a reduction in concentration of the
normally dominant hydrogen-peroxide producing lactobacilli and an increase in
concentration of other organisms, especially anaerobic gram negative rods [ 5-8 ]. The
major bacteria detected are Gardnerella vaginalis, Prevotella species, Porphyromonas
species, Bacteroides species, Peptostreptococcus species, and so many others.
Hydrogen-peroxide producing lactobacilli appear to be important in preventing
overgrowth of the anaerobes normally present in the vaginal flora. With the loss of
lactobacilli, pH rises and massive overgrowth of vaginal anaerobes occurs. These
anaerobes produce large amounts of proteolytic carboxylase enzymes, which break
down vaginal peptides into a variety of amines that are volatile, malodorous, and
associated with increased vaginal transudation and squamous epithelial cell exfoliation,
resulting in the typical clinical features observed in patients with BV. The rise in pH also
facilitates adherence of G. vaginalis to the exfoliating epithelial cells.
Amsel criteria for diagnosis of BV (at least three criteria must be present):
• Homogeneous, thin, grayish-white discharge that smoothly coats the vaginal walls
• Vaginal pH >4.5
• Positive whiff-amine test, defined as the presence of a fishy odor when a drop of 10
percent potassium hydroxide (KOH) is added to a sample of vaginal discharge
• Clue cells on saline wet mount ( picture 1A-B ). Clue cells are vaginal epithelial cells
studded with adherent coccobacilli that are best appreciated at the edge of the cell. For
a positive result, at least 20 percent of the epithelial cells on wet mount should be clue
cells. The presence of clue cells diagnosed by an experienced microscopist is the single
most reliable predictor of BV
Treatment of nonpregnant women
• Treatment of symptomatic women with bacterial vaginosis is indicated to reduce vaginal
discharge and odor. We recommend metronidazole orclindamycin ( Grade 1A ).
• Metronidazole 500 mg twice daily orally for 7 days
• Metronidazole gel 0.75 percent (5 grams) once daily vaginally for 5 days
• Clindamycin 2% vaginal cream or oral
• We recommend not treating sexual partners of women with BV ( Grade 1B )
. We treat symptomatic relapse with a longer course of therapy, using a different
antibiotic than that used for the initial episode. We suggest treatment of asymptomatic
women who are to undergo hysterectomy ( Grade 2B ).
Treatment of pregnant women
• Pregnant women with BV are at increased risk of preterm birth. We recommend not
screening all pregnant women for BV, given there is no evidence that screening and
treatment of asymptomatic infection reduces the risk of preterm birth ( Grade 1A ).
• Metronidazole or clindamycin are used in pregnant women

29. D. Placental dysfunction

the vignette is describing hypertension before 20 weeks of gestation which is not
considered gestational then there was proteinuria of 800 mg/day which means
hypertension with superimposed preeclampsia which causes placental insufficiency and
inappropriate amount of nutrients reach the baby with development of decreased
amniotic fluid as well.
B,C,E Fetal anomalies(probably if the patient received the regular prenatal care it would
have been diagnosed by now with the anomaly studies done as part of the routine care)
and U/S in first trimester is also part of the routine care so incorrect gestational age is
not probably incorrect either.

30. C. Cervisitis
Signs and symptoms — A significant proportion of women with cervicitis are
asymptomatic. Cervicitis in these women may be detected incidentally during physical
examination.
When present, symptoms are often nonspecific. All women have:
Purulent or mucopurulent vaginal discharge and/or
Intermenstrual or postcoital bleeding
Some women also have one or more of the following:
Dysuria, urinary frequency
Dyspareunia
Vulvovaginal irritation

New partner with the signs and symptoms suggest acute cervicitis.

31. D. Transvaginal incision and drainage

The history and exam goes with anatomical causes of primary amenorrhea- but NO U/S
or MRI done yet for further assessment(according to up to date if this is a vaginal
septum an ultrasound/MRI done next to assess if this is a thick or thin septum and
whether there is absent cervix or not to decide the type of operation, if it was an
imperforated hymen you can go immediately to incision and drainage but may be
because this is a pyohematocolpos you drain first???)
Imperforate hymen — An imperforate hymen is one of the most common obstructive
lesions of the female genital tract ( picture 1 ). At birth, infants may have a bulging
 introitus due to mucocolpos from vaginal secretions stimulated by maternal estradiol. If
the diagnosis is not made in the newborn period and the hymen remains imperforate, the
mucus will be reabsorbed and the child usually remains asymptomatic until menarche.
At that time, the adolescent girl may present with a history of cyclic abdominal or pelvic
pain and hematocolpos, which may give the hymenal membrane a bluish discoloration.
Marked distension of the vagina may also result in back pain, pain with defection, or
difficulties with urination.

Treatment —elliptical incision in the membrane close to the hymenal ring followed by
evacuation of the obstructed material.

Transverse vaginal septum — A transverse vaginal septum results when there is failure
of fusion and/or canalization of the urogenital sinus and müllerian ducts. These septa
may be located at various levels in the vagina The majority of transverse vaginal
septums have a fenestration and are thus not completely obstructed.
Clinical manifestations — The external genitalia appear normal, but internally the vagina
is shortened (a blind pouch if there is obstruction). Children may present with
mucocolpos, whereas adolescents can develop hematocolpos ( figure 6 ) or
pyohematocolpos due to an ascending infection through the small perforation. A mass
may be palpated above the examining finger on rectoabdominal examination.
Evaluation and treatment — Ultrasonographic or magnetic resonance (MR) imaging
helps to define the location and thickness of the septum and to differentiate between a
high septum and congenital absence of the cervix.
A small septum can be resected, followed by an end-to-end anastomosis of the upper
and lower vaginal mucosa. A thick septum is more difficult to excise and repair;
excision should be attempted only by surgeons experienced with this procedure.

32. D. Pyelonephritis
PRETERM LABOR CAUSES
It is usually difficult to identify the cause of preterm labor. Four general categories
causes include:
Uterine bleeding — Conditions like placenta previa (when the placenta partially or
completely covers the cervix) and placental abruption (when the placenta separates from
the uterus before delivery) can cause the fetal membranes to rupture prematurely and
can trigger preterm labor.
Stretching of the uterus — Having twins, triplets, or more, or having polyhydramnios (an
excessive amount of amniotic fluid around the baby) causes stretching of the uterus,
which can lead to uterine contractions and preterm labor.
Bacteria or inflammation — Bacteria or inflammation caused by an infection in the uterus
can stimulate the production of substances that trigger uterine contractions.
Physical or psychological stress — Severe stress can lead to the release of hormones
that cause uterine contractions and preterm labor.
A. chorioamnionitis you will need to have history of either PPROM, uterine tenderness
and other features
 B.CLINICAL FINDINGS OF Cervical insuffiecieny
Past obstetrical history — The past obstetrical history of women with cervical
insufficiency is characterized by:
●History of second-trimester pregnancy losses/deliveries, often associated with a short
labor
●History of progressively earlier deliveries in successive pregnancies
Symptoms — Women with cervical insufficiency may be asymptomatic or may present
with mild symptoms, such as pelvic pressure, premenstrual-like cramping or
backache, and/or a change in the volume, color, or consistency of vaginal discharge.
Volume may increase; color may change from clear, white, or light yellow to pink, tan, or
spotting; and consistency may become thinner. These symptoms may begin between 14
and 20 weeks of gestation and may be present for several days or weeks before
diagnosis of cervical insufficiency.
Contractions are absent or mild.
Physical examination — The initial clinical examination may reveal a soft, somewhat
effaced cervix, with no or minimal dilation [10]. Provocative maneuvers such as
suprapubic or fundal pressure or the Valsalva maneuver may reveal fetal membranes in
the endocervical canal or vagina; this is always an abnormal finding. Tocodynamometry
shows no or infrequent contractions at irregular intervals.
Late clinical presentation is characterized by advanced dilation and effacement (eg, ≥4
cm dilated and ≥80 percent effaced), spotting, unprovoked grossly prolapsed
membranes or ruptured membranes, or contractions that seem inadequate to explain the
advanced effacement and dilation.
Imaging — The cervix may be short (below the 10th percentile [25 mm]), the fetal
membranes may be separated, and debris (sludge) may be seen in the amniotic fluid. A
rapid rate of decrease in cervical length over time [11] and cervical shortening before 20
weeks [12-14] may be noted. (See "Second-trimester evaluation of cervical length for
prediction of spontaneous preterm birth", section on 'Technique'.)
Also the signs and symptoms of preterm labor should not be attributed to any of the
causes mentioned earlier to support the diagnosis of cervical insufficiency

33. F. Endometriosis (Typical history findings)

34. N. Ruptured corpus luteal cyst
Culdocentesis may be used to evaluate women with pain in the
lower abdomen/pelvis to determine whether intraabdominal fluid is present and, if
present, to reveal the nature of the fluid (eg, serous, purulent, bloody). Thus, the
procedure can be helpful in evaluating women with a suspected ruptured ovarian
cyst, pelvic inflammatory disease, or ruptured ectopic pregnancy
Ultrasound examination has largely replaced culdocentesis because it accurately
identifies the presence of abdominal/pelvic fluid, is more comfortable for the patient, and
provides additional information about the pelvis, such as whether there is an adnexal
mass or intrauterine pregnancy. Culdocentesis may be useful when ultrasonography is
not readily available.
 INTERPRETATION OF FINDINGS — Subsequent steps depend upon type of aspirated
fluid.
• A small amount of clear fluid is normal. Copious peritoneal fluid suggests a ruptured
fluid filled cyst or ascites.
• No fluid in the posterior cul-de-sac can also be a normal finding. However, a dry tap is
considered unsatisfactory and suggests that the needle tip is obstructed by tissue due to
poor positioning, adhesions, or other pathology.
• Nonclotting blood indicates active intraperitoneal bleeding. Determine the hematocrit: A
hematocrit over 15 percent is most consistent with hemorrhage from a ruptured ectopic
pregnancy or actively bleeding ruptured corpus luteum while a hematocrit less than 8
percent is more consistent with blood tinged fluid from a ruptured ovarian cyst or pelvic
inflammation.
• Clotting blood suggests blood from a vein or artery may have been aspirated. The most
common site of vessel perforation is the uterine vein. Remove the needle, reinsert a new
needle, and aspirate again.
• The presence of pus indicates an infectious process, possibly as abscess.

Rupture of an ovarian cyst may be asymptomatic or associated with the sudden onset of
unilateral lower abdominal pain. The pain often begins during strenuous physical activity,
such as exercise or sexual intercourse. It may be accompanied by light vaginal bleeding
due to a drop in secretion of ovarian hormones and subsequent endometrial sloughing.
Blood from the rupture site may seep into the ovary, which can cause pain from
stretching of the ovarian cortex, or it may flow into the abdomen, which has an irritant
effect on the peritoneum. However, it is also possible for large amounts of blood to be
present in the abdomen without producing symptoms. Serous or mucinous fluid released
upon cyst rupture is not very irritating; the patient may remain asymptomatic despite
accumulation of a large volume of intraperitoneal fluid. On the other hand, spillage of
sebaceous material upon rupture of a dermoid cyst causes a marked granulomatous
reaction and chemical peritonitis, which is usually quite painful.

Ovarian torsion — Lower abdominal pain and an adnexal mass are the most common
findings associated with ovarian torsion. Nausea and vomiting frequently accompany
torsion, but are less common with cyst rupture. Imaging studies, particularly Doppler
velocimetry, can help distinguish the two disorders, but the presence of a cystic or
solid adnexal mass and free fluid in the posterior cul-de-sac are common with both
entities this is just to make the answer confusing 

35. C. Amnioinfusioin
Variable deceleration — A variable deceleration reflects the fetal autonomic reflex
response to transient mechanical compression of the umbilical cord. Initially,
compression of the umbilical cord occludes the thin-walled, compliant umbilical vein,
decreasing fetal venous return and triggering a baroreceptor-mediated reflex rise in FHR
(sometimes referred to as a "shoulder"). Further compression occludes the umbilical
 arteries, causing an abrupt increase in fetal peripheral resistance and blood pressure.
Baroreceptors detect the abrupt rise in blood pressure, triggering an increase in
parasympathetic outflow and an abrupt decrease in heart rate. As the cord is
decompressed, this sequence of events occurs in reverse.
Cord compression with or without other sources of disruption of fetal oxygenation may
result in recurrent variable decelerations with absent/minimal variability and no
accelerations. Prompt attention is required because ongoing hypoxic injury cannot be
excluded.
Amnioinfusion — Amnioinfusion, the instillation of isotonic fluid into the amniotic cavity, has
been advocated to improve neonatal outcome in women laboring with thick meconium in the
amniotic fluid. The proposed benefits of amnioinfusion include dilution of thick clumps of
meconium by the instilled fluid, and possible prevention or relief of cord compression. The fetal
heart rate should be monitored continuously to determine whether the variable decelerations
resolve and to identify the occurrence of new nonreassuring fetal heart rate patterns. However,
amnioinfusion is not beneficial in reducing meconium-related neonatal morbidity, with the possible
exception of settings with limited facilities to monitor the fetus during labor [3]. As a result,
amnioinfusion is not recommended as a routine approach for mothers with meconium-stained
amniotic fluid
A. Technique for breech presentation and this delivery has vertex presentation
B. Forceps use requires full dilatation of the cervix to begin with then the rest of indications like
prolonged 2nd stage or fetal heart deccelarations and so on.
D. Amniocentesis ?? E. Cordocentesis ?? they seem totally far away from this situation
36. C. 50%
Sickle cell is autosomal recessive, she has hb S and her husband has sickle cell trait
which means that one sickle anemia gene will be definitely taken from the mother and
the other gene will be a 50% chance taken from father and the overall probability is 50%

Electrophoresis: The reference ranges are as follows: NORMAL [1]

HbA 1 : 95%-98%
HbA 2 : 1.5%-3.5%
HbF: < 2% (age-dependent)
HbC: Absent
HbS: Absent

Presence of HbS, but with a higher proportion of HbA than HbS: Sickle cell trait (HbAS)
or sickle α-thalassemia
Presence of HbS and HbF, but no HbA: Sickle cell anemia (HbSS), sickle beta 0 -
thalassemia (hereditary persistence of fetal hemoglobin [HPFH]), or sickle–HPFH
Overall higher proportion of HbS than HbA and HbF: Sickle beta + -thalassemia (most
likely)
Presence of HbC, but with a higher proportion of HbA than HbC: HbC trait (HbAC)
Presence of HbC and HbF, but no HbA: HbC disease (HbCC), HbC –beta 0 -thalassemia
(HbC-HPFH)
A higher proportion of HbC than HbA: HbC beta + -thalassemia
Presence of HbS and HbC: HbSC disease
 Presence of HbH: HbH disease
Increased HbA 2 : Beta-thalassemia minor
Increased HbF: Hereditary persistence of fetal hemoglobin, sickle cell anemia, beta-
thalassemia, HbC disease, HbE disease

37. B. Duplex ultrasonography

38. B. Hb Electrophoresis

39. A
Serum markers for epithelial ovarian carcinoma — Serum CA 125 is the most commonly used
laboratory test for the evaluation of adnexal masses for EOC. In our practice, we measure CA
125 in all postmenopausal women with an adnexal mass. In premenopausal women, we measure
a serum CA 125 only if the ultrasound appearance of a mass raises sufficient suspicion of
malignancy to warrant a repeat ultrasound or surgical evaluation. Biomarkers that are used to
decide whether to refer a patient with suspected EOC to a gynecologic oncologist are OVA1 and
the Risk of Malignancy Algorithm

40. D. Testosterone (Hyperandrogenic state, could be PCOS and even if not testosterone
is still the answer in this case).

41. J. Vasa Previa

The prenatal diagnosis of velamentous cord insertion is based upon the presence of
characteristic sonographic findings (splayed, membranous umbilical vessels with no
Wharton’s jelly) at the placental umbilical cord insertion site. A definitive diagnosis of
velamentous cord insertion is made by pathologic examination of the placenta, cord, and
membranes after delivery. ●The prenatal diagnosis of vasa previa is based upon
characteristic sonographic findings (membranous vessels that cross the internal cervical
os). In the absence of prenatal sonographic diagnosis, a clinical diagnosis of vasa
previa should be suspected in the setting of vaginal bleeding that occurs upon
rupture of the membranes and is accompanied by fetal heart rate abnormalities,
particularly a sinusoidal pattern or bradycardia. Fetal exsanguination can occur
within minutes.
●In the second trimester, transvaginal ultrasound examination to look for vasa previa is
reasonable in pregnancies with: velamentous cord insertion; conceived following use of
assisted reproductive technologies; low-lying placentas, placenta previa, or bilobed or
succenturiate lobe placentas in the lower uterine segment; and multiple gestations. We
suggest both ultrasound examination and color Doppler of the umbilical cord insertion
site.
Velamentous umbilical cord:
●The vessels in a velamentous umbilical cord are at increased risk of compression
compared to a normal cord. We suggest fetal heart rate monitoring to detect
compression of cord vessels beginning at 36 weeks of gestation.
●There is no evidence that induction of labor or scheduled cesarean delivery improve
the outcome of pregnancies complicated by velamentous cord insertion without vasa
previa. We continuously monitor the fetal heart rate during labor and exercise caution
when exerting traction on the umbilical cord after birth
●The frequency and severity of cord compression may be higher for vasa previa than
velamentous umbilical cord (without vasa previa); therefore, we monitor pregnancies
with vasa previa more closely. We suggest twice weekly nonstress testing beginning at
28 to 30 weeks, with hospitalization at 30 to 32 weeks of gestation for more frequent
monitoring to detect early evidence of cord compression. Hospitalization also facilitates
the ability to perform an emergency cesarean delivery in the event of premature rupture
of membranes or preterm labor. (See 'Antepartum' above.)
● Delivery — We deliver the fetus by emergency cesarean delivery if any of the
following occur:
●Labor
●Premature rupture of membranes
●Repetitive variable decelerations refractory to tocolysis
●Vaginal bleeding accompanied by fetal tachycardia, a sinusoidal heart rate pattern, or
evidence of pure fetal blood by Apt test or Kleihauer-Betke assessment
There are no high-quality data on which to base a recommendation for optimal timing of
scheduled delivery. We generally agree with the authors of large series and decision
analyses who have recommended delivery at about 35 weeks of gestation, without
assessment of fetal lung maturity [50,56]. The Society for Maternal-Fetal Medicine
Consult Series concluded planned cesarean delivery because of vasa previa is
reasonable at 34 to 37 weeks of gestation [34]. Type O negative blood should be
available for emergency transfusion of a severely anemic newborn, when clinically
indicated.
Ideally, the hysterotomy should avoid aberrant blood vessels. If a fetal vessel is
lacerated inadvertently during delivery, the cord should be clamped immediately to
preventfetal/neonatal blood loss [34].
42. E. Colonoscopy

43. D. Uteroplacental Insufficciency

This subject is covered by most sources and maybe skipping to the paragraph
“LATE DECELRATIONS” is good for those who do not have time to read details.

CATEGORY I TRACINGS: DEFINITION AND MANAGEMENT —

●Baseline rate: 110 to 160 beats per minute (beats per minute [bpm])
●Moderate baseline fetal heart rate (FHR) variability (amplitude 6 to 25 bpm)
●No late or variable decelerations
●Early decelerations may be present or absent
●Accelerations may be present or absent
Category I electronic fetal monitoring (EFM) tracings are considered “normal” because
studies have demonstrated that these findings are associated with the absence of fetal
metabolic acidemia at the time of observation [7-10]. No intervention is indicated.
CATEGORY III TRACINGS: DEFINITION AND MANAGEMENT — A category III tracing
is defined by either of the following criteria:
●Absent baseline fetal heart rate (FHR) variability and (any of the following):
•Recurrent late decelerations
•Recurrent variable decelerations
•Bradycardia
OR
●A sinusoidal pattern

A category III tracing is “abnormal” because studies have demonstrated that these
findings are associated with an increased risk of fetal hypoxic acidemia, which can lead
to cerebral palsy and neonatal hypoxic ischemic encephalopathy
Therefore, when a category III pattern is identified, preparations for delivery should be
made while initiating resuscitative measures to improve uteroplacental perfusion and
oxygen delivery. (See 'In utero resuscitation' below.) If in utero resuscitation leads to
resolution of the category III tracing, cesarean delivery can be averted.
Scalp stimulation to provoke FHR acceleration should be attempted. In general, when
scalp stimulation induces an acceleration, the probability of fetal acidosis is less than 10
percent versus about 50 percent when no acceleration occurs in this setting. The time
from the decision to delivery should consider the health of both mother and fetus: there
may be circumstances (eg, difficult maternal airway, maternal coagulopathy, severe
obesity) where safe delivery cannot be performed expeditiously.
In utero resuscitation — for management of category II and III tracings
●Reposition the patient onto her left or right side
●Administer oxygen (eg, 8 to 10 L/min of oxygen via nonrebreather mask)
●Administer an intravenous (IV) fluid bolus (eg, 500 to 1000 mL of lactated Ringer's or
normal saline solution)
●Discontinue uterotonic drugs
●Administer a tocolytic drug (eg, terbutaline 250 mcg subcutaneously)
●For patients who were recently given epidural drugs for labor pain, ask the anesthesia
team to evaluate the patient for administration of an alpha-adrenergic agonist
(eg, phenylephrine, ephedrine) to reduce sympathetic blockade

CATEGORY II TRACINGS: DEFINITION AND MANAGEMENT — Category II fetal heart

rate (FHR) tracings include all FHR patterns that are not classified as category I (normal)
or category III (abnormal)

Late decelerations without loss of variability or accelerations — Recurrent late

decelerations are caused by a reflex central nervous system (CNS) response to fetal
hypoxia and acidemia, as well as direct myocardial depression and humoral factors [49].
Fetal hypoxia leading to late decelerations may occur in the following settings:
●Uterine tachysystole
●Maternal hypotension
●Maternal hypoxia
●Maternal vasculopathy
●Placental disorders associated with placental insufficiency
Assessment of FHR variability and accelerations should be part of the evaluation of
recurrent late decelerations, given the low predictive value of late decelerations alone for
fetal acidosis and poor neonatal outcome [50-52]. Moderate variability is strongly
associated (98 percent) with an umbilical pH >7.15 [43] and spontaneous or elicited FHR
accelerations are strongly associated with pH>7.10 [17-20].

Fetal tachycardia — Fetal tachycardia is defined as a baseline FHR greater than 160
bpm for at least 10 minutes. Causes of fetal tachycardia include:
●Maternal-fetal infection
●Medications (eg, beta-agonists, atropine, cocaine)
●Maternal hyperthyroidism
●Placental abruption
●Fetal hypoxia
●Elevated maternal catecholamine levels
Rarely, fetal tachycardia can be due to a fetal tachyarrhythmia, such as atrial flutter or
supraventricular tachycardia. These tachyarrhythmias are characterized by a very high
FHR, often in excess of 200 bpm. Fetal tachycardia less than 200 bpm alone has not
been strongly associated with fetal acidemia, unless associated with recurrent
decelerations, absent accelerations, orminimal/absent variability [53-56].
The evaluation of fetal tachycardia should include assessment for maternal
infection or abruptio placentae and a review of maternal medications. Appropriate
treatment should be initiated if the underlying cause can be identified and treated
(eg, acetaminophen for reduction of fever and antibiotics for treatment of intraamniotic
infection). In addition, fetal scalp stimulation should be performed to provoke FHR
acceleration, which is a sign that the fetus is not acidotic. Delivery is indicated if
acidemia or placental abruption is suspected. Tachycardia due to chorioamnionitis is
generally not an indication for delivery unless decelerations or category III tracing, or if
the patient is remote from delivery and the tachycardia is unable to be resolved with
maternal hydration and antipyretic therapy.

Variable decelerations without loss of variability or accelerations — Variable

decelerations occur when the umbilical cord is compressed. Intermittent variable
decelerations (associated with <50 percent of contractions) are frequently observed
intrapartum and usually associated with moderate variability and/or accelerations. They
do not typically result in adverse consequences, presumably because transient cord
compression is well tolerated by the fetus [57]. Thus, they do not require intervention.
Metabolic acidosis or mixed metabolic and respiratory acidosis can develop, however,
with increasing duration, depth, and frequency of variable decelerations [58]. Therefore,
recurrent variable decelerations (>50 percent of contractions) require close surveillance
for loss of variability and accelerations, which signify a category III tracing. In utero
resuscitation measures are indicated, with the major focus to resolve cord compression.
Change of maternal position is a reasonable first treatment option [25] and
amnioinfusion is a reasonable second-line option. Patients with low pre-amnioinfusion
amniotic fluid volume are most likely to experience resolution of variable decelerations;
in patients with a high amniotic fluid volume (amniotic fluid index >12 cm) and variable
heart rate decelerations, a nuchal cord or umbilical cord knot is a more likely cause of
the variable pattern than reduced amniotic fluid so amnioinfusion is less likely to be
beneficial [60]. (See "Amnioinfusion: Technique".)
Delivery is indicated if a category III tracing develops.

Loss of variability without decelerations — FHR variability results from oscillatory

input by the parasympathetic nervous system. The new onset of minimal variability
(amplitude 0 to 5 bpm) may occur for several reasons, including [61-63]:
●Fetal sleep cycle - These cycles generally last approximately 20 minutes, but may
persist for as long as one hour. When the fetal sleep cycles are over, moderate
variability should return.
●CNS depressants - The most common medications that decrease variability are opioids
and magnesium sulfate. The effect of maternal opioids on FHR variability generally lasts
no more than two hours.
●Fetal hypoxemia
If the FHR pattern had been normal and there are no decelerations, a reasonable
approach to the assessment and management of new onset minimal fetal variability is to
make a presumptive diagnosis of a fetal sleep cycle or the effect of recently
administered maternal medications. Both of these causes warrant expectant
management. It is also prudent to attempt to induce accelerations with scalp stimulation,
as the presence of accelerations is strong evidence of the absence of fetal acidemia at
that time [18]. A maternal fluid bolus, repositioning, and/or maternal oxygen
administration are appropriate adjunctive measures (table 2B), especially in settings in
which a benign etiology is less certain, such as coexistent pregnancy complications
associated with uteroplacental insufficiency.
Long-standing loss of variability can be related to congenital or acquired anomalies of
the CNS or heart, or to very preterm gestation [64-66].

Fetal bradycardia/prolonged deceleration without loss of variability — Fetal bradycardia

(below 110 bpm) or a prolonged deceleration (table 1) is approached in a similar way
clinically, since the distinction between these two entities is based primarily on the
number of minutes of the decrease in FHR. The causes of prolonged deceleration or
fetal bradycardia include:
●Rapid fetal descent
●Cord prolapse
●Placental abruption
●Maternal hypotension
●Uterine rupture
●Tachysystole
If variability and accelerations are present when the FHR returns to a normal baseline
rate, fetal acidemia is unlikely.
Treatment of fetal bradycardia or prolonged deceleration is aimed at the cause.
Evaluation should include assessment of maternal blood pressure and contraction
 frequency and strength, and physical examination for evidence of rapid fetal descent,
cord prolapse, placental abruption, or uterine rupture. (See "Umbilical cord
prolapse"and "Rupture of the unscarred uterus" and "Placental abruption: Clinical
features and diagnosis" and "Uterine rupture after previous cesarean delivery".)
Delivery is indicated if resuscitative measures to correct the underlying cause are not
possible or fail to resolve the bradycardia. In one study of 5388 term, singleton
pregnancies at full dilation with a non-anomalous fetus in cephalic presentation, a
terminal deceleration occurred in 951 (17.7 percent) and only 12 (1.3 percent) had
umbilical cord gas arterial pH <7.10 [67]. Of the 31 who had terminal bradycardia (FHR
<110 bpm for ≥10 minutes before delivery), 4 had an umbilical cord gas arterial pH
≤7.10. Although infants with terminal bradycardia were at increased risk of acidemia, the
positive predictive value was only 12.9 percent. The authors also noted a positive
association between increasing duration of a terminal deceleration beyond two minutes
and decreasing pH (pH decreased by 0.042 for every additional two minutes after the
first two minutes).
Delivery is also indicated for development of a category III tracing.
44. B. Fetal Sleep Cycle
although if this heart pattern is seen for 5 hours I am not sure what the answer would
be(see explanation of previous answer)
A. Chorioamnionitis has different pattern of presentation
D. Cord compression causes variable decelerations
E. Uteroplacental insufficiency causes late decelartions
45. A. Breast cancer

B. Cervical Cancer Risk factors — The two major histologic types of cervical cancer,
adenocarcinoma and squamous cell carcinoma, and the preinvasive disease]. Most of
these are associated with an increased risk of acquiring or having appropriate
compromised immune response to infection with HPV.
●Early onset of sexual activity
●Multiple sexual partners
●A high-risk sexual partner (eg, a partner with multiple sexual partners or known HPV
infection)
●History of sexually transmitted infections (eg, Chlamydia trachomatis, genital herpes)
●History of vulvar or vaginal squamous intraepithelial neoplasia or cancer (HPV infection
is also the etiology of most cases of these conditions)
●Immunosuppression (eg, human immunodeficiency virus infection)

Cervical cancer is less common in sexual partners of circumcised males [13]. Early age
at first birth (younger than 20 years old) and increasing parity (3 or more full term births)
are also associated with an increased risk of cervical cancer; these are also likely due to
exposure to HPV through sexual intercourse [12].
Low socioeconomic status is associated with an increased risk of cervical cancer.

Oral contraceptive use has been reported to be associated with an increased risk of
cervical cancer.
In contrast to squamous cell cancer of the cervix, cigarette smoking is not associated
with a significantly increased risk of adenocarcinoma of the cervix
C. Endometrial

E. Ovarian
46. C. Increasing her current anticonvulsant medication
Drug levels and dose adjustment — Pregnancy is accompanied by many alterations in
drug metabolism, including increased liver metabolism, renal clearance, and volume of
distribution, and decreased gastrointestinal absorption and plasma protein binding
[20,30-32]. As an example, for antiseizure drugs that are highly protein bound
(eg, phenytoin, valproate), the total plasma drug level may decrease with impaired
protein binding, but the physiologically important free or unbound drug concentration
may not change. As a result, free drug levels for these antiseizure drugs may be more
reliable during pregnancy. However, medication dosage should be adjusted if the
patient's seizures are not controlled, not because the free or total level has decreased.
Both total and free plasma drug levels, where available, should be checked at weeks five
to six and week 10 to evaluate the environment for organogenesis, and then at least
once each trimester. Antiseizure drugs that may warrant closer monitoring
include lamotrigine, levetiracetam, oxcarbazepine, phenytoin andtopiramate [11]:
47. D. Prostaglandin production
Primary dysmenorrheal: due to prostaglandin, a very similar question present in
UWorld no. 2395 (6547482)
48. C. Stress Incontinence
49. K. Septic abortion
50. Uteroplacental artery
According to up to date the Factor V leiden deficiency has not proved to be correlated
with early pregnancy losses but there is a correlation with late pregnancy losses due to
placental thrombosis and infarction and in this question the only related answer to this
piece of information is uteroplacental artey (spiral arteries convert to uteroplacental
arteries in pregnancy)