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 d one 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 b eneficial for advanced tumors not cured by surgery and radiation. 4. G. Uterine Synechiae. (Asherman syndro me) 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 Placent a 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 Ad van ced mat ern al age a ge Infertility treatment Previous abortion Previous intrauterine surgical procedure Materna Ma ternall smoking
Maternal cocaine use Male fetus Non-white race
6. D. UTD states that Arrest of labor is diagnosed at cervical dilation ?6 cm in a patient with ruptured 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 i s 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. Va Vaginal ginal 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 rela tive risk of fracture is in individuals with osteoporosis, the absolute number of fractures in those with BMD Tscores in the low bone mass (osteopenia) range is the same or greater than in those with T-scores in the osteoporosis range. ASSESSMENT ASSESS MENT OF FRACTURE FRACTURE RISK — Screening for osteoporosis involves involves fracture risk assessment and measurement of BMD. Most fractures occur in women and men who do not have osteoporosis o steoporosis 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 i mmediate psyc hiatri c 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 Restri cti on The main impact on the fetus is undernutrition as a result of utero-placental vascular insufficiency, which leads to growth retardation. 12. E. Normal L abor 13. A. Detrus or 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 rel iability 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, 0.360.62) [ 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 urin ary 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 (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 Postvoid residual volume
14. F. Vesic ovaginal f ist ula 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 papi llomas 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 Synd rome 17. E. IUD — 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. Effectiveness
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 Synd rome 20. A. Use Lubric ant In the postpartum period, estrogen levels decline secondary to the loss of pla cental 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 u rinary 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. Condylo mata Acum inata 23. A. Amenorrhea Risk of overzealous sharp curettage is Asherman syndrome 24. A. Atelectasis 25. B. Increased cervical cell vuln erability to in fections 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 tracho matis i nf. 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. Pedunc ulated subm ucou s leiomy oma 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. Am sel cr it eri a for di agn os is 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 d iagnosed 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 or clindamycin ( 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 • • •
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We recommend not treating sexual partners of women with BV ( Grade 1B ) . We treat symptomatic relapse with a long er 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 dys func tion 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 reg ular 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. Cervisi tis 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. Transv aginal inc isio n and dr ainage 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. Pyelonephri tis 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 abru ption (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 labo r. 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 i rregular 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 t he diagnosis of c ervical insufficiency 33. F. Endometriosis (Typical his tory findings) 34. N. Ruptured co rpus l uteal 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.
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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 i t 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 jus t 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. Am ni oi nf us io n — 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 o ccurrence 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 no t 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 nd prolonged 2 stage or fetal heart deccelarations a nd 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, betathalassemia, HbC disease, HbE disease 37. B. Duplex ultrason ography
38. B. Hb Electrop horesis
39. A Serum markers for epithelial ovarian carcinom a — 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 Prev ia 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 pr enatal sonographic d iagnosis, 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 sinusoid al pattern or br adycardia. 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 fr equency 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 no nstress 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 abo ut 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. Colonos copy
43. D. Uteroplacental Insu ffi cci ency This subject is covered by most s ources and maybe skipping to the paragraph “ LATE DECELRATIONS” is goo d for t hose who d o not have tim e 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 ob servation [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 deceleration s 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 insuff iciency
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 a ssociated with recurrent decelerations, absent accelerations, orminimal/absent variability [53-56]. The evaluation of f etal tachycardia should include assessment for maternal infection or abruptio placentae and a review of maternal m edications. 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 v ariability 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 a nd/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 w ithout decelerations — FHR variability results from oscillatory input by the parasympathetic nervous system. The new onse t 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 Cyc le 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 c ancer
B. Cervic al Cancer Risk f actors — 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 ri sk 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 drug s 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 dy smenorrheal: due to prostaglandin, a very si milar question pr esent in UWorld no. 2395 (6547482) 48. C. Stress Incont inence 49. K. Septic abortio n 50. Uteroplacental art ery 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)
