ࡱ> 5@ bjbj22 (XX"l::::,:t;;;;;Q=Q=Q=޾$WRH]?=@Q=??;;aWWW?;;޾W?޾WWW;h; @ X:Q6Nw0ܺU&8Q==^W3>L>ZQ=Q=Q=3d5$W d52003 Main A 38-year-old nulliparous woman is now 10 weeks pregnant after a successful IVF treatment with a singleton pregnancy. She is very worried about foetal/ chromosomal abnormalities. Describe how you would manage this woman. Outline: Introduction- many ways to determine chromosomal and fetal abnormalities- each with its own pros n cons. Screening tests vs diagnostic tests As for this patient, she is 38 years old(Advances maternal age), therefore risk of chromosomal abnormality is roughly 1/240 to 1/00. Also, mention that this is a very valuable pregnancy s patient is 38, nulliparous and conceived thru ivf, suggesting some degree of subfertility. IVF per se does not increase risk of abnormalties but the patient has to be assess for other risks of abnormalities such as GDM,alcohol intake, previous abnormal pregnancy or stillbirth, family history of chromosomal/foetal abnormalities(Downs etc) Chronologically, at 10 weeks only a few tests can be performed. At 10-14 weeks, ultrasound can be done to look at nuchal translucency and thickness. It is a screening test and only has 80% sensitivity. Other features can be sought for during this scan such as absense of nasal bone, duodenal atresia which would be suggestive of Down;s syndrome. However, it is operator dependent. Chronic villus sampling is a diagnostic test which can be done at 10-12 weeks. Method:trophoblastic tissue is sampled either transcervically or transabdominally, once the placenta has been located by ultrasound. Cells from the villi tissue sample are allowed to grow in special lab conditions for several days and are then analyzed. Because the placenta and fetus develop from the same fertilized egg, the genetic material is usually the same. That's why CVS provides a good indication of the health of the fetus. However, CVS has a 3% risk of spontaneous abortion(1% procedural risk, 2% risk of spontaneous abortion (as risk at 10 weeks quite high). Other complications include limb reduction of fetus. Screening tests such as triple tests are non-invasive and therefore favourable. Serum b-hcg,afp, estriol levels (high hcg, low afp and estriol suggestive of Downs syndrome). However, it has a false positive of 4.5% and is not diagnostic. It gives an age specific risk, from which invasive diagnostic tests can we performed as age related risk + screening risk outweighs risk of miscarriage. In women over 35-like this patient- diagnostic tests are offered straight away as the age related risk is alone high enough to outweigh risk of miscarriage. 2nd trimester Screening: ultrasound (16-20weeks) scan to look for fetal structural abnormalities. Structures better seen at this period, therefore malformations can be picked up with greater confidence. Once again, this is operator dependent. Certain stru abnormalities like absence of nasal bone,duodenal atresia, hydronephrosis, short femur chroid plexus cysts and enlarged ventricles are suggestive of Downs syndrome. Diagnostic:Amniocentesis can be done in the 2nd trimester. It has a lower risk of spontaneous abortion than cvs(0.3%).It is a technique by which a fine needle is placed transabdominally into amniotic cavity under u/s guidance and done btwn 15-20 weeks when fetal sqaumous cells shed in fluid can be collected via amnio can be cultured and karotyped and studied for chromosal abnormalities. Complications are amninotis (1in1000), fetal injury, bowel,vascular injury, Rh sensitization. Cordocentesis is another diagnostic test which can only be done after 20 weeks, up t o40 weeks. It is done transabdominally under u/s guidance and fetal blood is sampled from the umbilical cord. Fetal white blood cells can be cultured karyotyped in 24-48hrs, earlier than the other tests. Risk of miscarriage is 1%. b) She decided on an amniocentesis and the result revealed a karyotyping of Trisomy-21. She is now 19 weeks pregnant. Describe your management Introduction..say that children with trisomy 21 chromosomal abnormality have a downs syndrome phenotype. Options available to the patient are either continuing with the pregnancy or aborting it. Before she decides, she must be counseled by doctors, as well as social workers. The incidence of Downs synd is about 1/650 livebirths. Also she has to be informed that there is a higher risk of spontaneous miscarriage as her fetus has a chromosomal abnormality. Medical complications related to Downs synd are congenital heart defects(asd,vsd,pda) and hence may require reparative cardiac surgery which can be costly. The will also require antibiotic prophylaxis before invasive procedures to prevent infective endocarditis. Duodenal atresia, acute myeloid leukemia, alzhemers at an early age Mental retardation- mean iq 40 to 50 Short stature Shortened life span 50% expectancy of 50 Social problems such as integrating into society, performing activities of daily living. The medical social worker should also make known the resources available for a child with Downs synd- such as special schools. If she decides to abort, it should be an informed decision after being informed of the risks of abortion and the risks of recurrence of Downs in the next pregnancy. Abortion is 2nd trimester can be surgical or medical. Medically, prostaglandins(extra/intra amniontic), iv oxytocin together with RU486 P.O can be given. Surgically, dilatation n evacuation, hysterotomy or hysterectomy can be done. In this patients case, medical abortion would be preferred as it carries a lower surgical and anaesthetic risk. Surgical D&E is safe provided there is sufficient cervical preparation(prostin?), operator experience and u/s guidance. In surgical option chosenPreoperatively, they should have an ultrasound scan, rhesus status(anti-d administered if necessary) and psychological couselling. Intraoperatively, they should be given antibiotic prophylaxis. Counselling for recurrence of Downs in future pregnancy Trisomy 21 can happen because of non-disjunction(95%), robertsonian translocation(3%) or 2% mosaicism. Therefore, karyotyping( and FISH?) should be done to determine what the abnormality is. If it is non-disjunction, risk of recurrence is 1% higher than the age specific risk. If the translocation is denovo(happening at or prior to conception i.e both father n mother are normal)..risk is 2-3% If mother is balanced carrier..15% If father.. <5% If there is a 21:21 robertsonian translocationall the offspring will have downs syndrome. Also, she has to decide if she wants to abort by 24 weeks. After which it is considered illegal, or only legal subject to approval by ethics committee. The patient is a 34-year-old Gravida 5 Para 4. She has been followed up in the antenatal clinic since the first trimester. She is now 32 weeks and the baby is in a breech presentation. Discuss the management of this patient from now until delivery. Issues from Hx: 1) breech presentation 2) multiparous Intro: Incidence of breech 20% at 28 weeks; 3% at term. ( chance of spontaneous turning. 3 types of breech. Frank, Complete, Incomplete Significance of breech ( 4 times higher risk of perinatal mortality and neonatal morbidity. Early Antepartum Mx (<34 wk) confirm dx of breech presentation: PE, U/S cause of breech Hx: multiparicity, certainty of dates (prematurity is major cause), multiple pregnancy, recurrence? PE: multiple pregnancy, poly/oligohydramnios U/S: congenital malformations, uterine abnormalities, dating fetus, placenta previa Spontaeneous version: assume knee-chest position for 5-10min/day when she experiences strong kicks ( Four randomised trials have been undertaken to establish whether or not postural management (knee-chest position) is effective in converting breech to cephalic presentations. In these studies no significant benefits were found. Mid Antepartum Mx External cephalic version ( after 37th week and before onset of labour. Before 37th week should NOT be done, cos of tendency to revert to breech and a resultant iatrogenic prematurity if a cx occurs during the process. ECV has been subjected to rigorous scientific appraisal in six randomised controlled trials. There is significant reduction in the risk of caesarean section in women where there is an intention to undertake ECV (odds ratio 0.4; 95% confidence intervals 0.3-0.6) without any increased risk to the baby. Process: tocolysis to relax uterus + transabdominal manipulation under U/S guidance. Equipped to perform emergency caesarean in event of Abruption Cord compression Contraindications: UPI, hypt, IUGR, oligohydramnios, previous uterine surgery Successful ECV ( delivery by NVD Contraindications to ECV or failed ECV ( choice of LSCS or trial of vaginal delivery Late Antepartum Decide mode of delivery and time. Clnical pelvimetry to ensure no cephalopelvic disproportion. Xray pelvimetry not shown to be superior. For a term breech, obstetrical consensus (RCOG) supports vaginal delivery of selected cases provided that management protocols are strictly adhered to. If the management criteria cannot be satisfied, elective CS is indicated. LSCS Premature breeches should be delivered by elective caesarean due to large fetal head being easily trapped at cervix. Incomplete breeches are delivered by caesarean. If trial of vaginal delivery is contraindicated cephalopelvic disproportion PP Previous LSCS Macrosomia Preterm Trial of Vaginal delivery There are three possible methods by which a vaginal delivery can be achieved: spontaneous breech delivery - the infant is born with support of the trunk but without traction or manipulation; assisted breech delivery (preferred technique) - spontaneous delivery of the breech up to the level of the umbilicus followed by obstetrician-assisted delivery of the shoulders and aftercoming head and, total breech extraction - the obstetrician extracts the entire body of the infant. This method of delivery is unacceptable for a term singleton breech. Criteria: frank or complete breech gestation >36 wk 2.5 3.8 kg fetal head must be flexed no fetopelvic disproportion No other indication for caesarean Intrapartum Mx Anticipate cord prolapse, compression, hypoxia ( Emergency LSCS Multiparity Increased risk of CPD Iron, folate supplements Increased risk of intrapartum, postpartum haemorrhage Family planning: contraception/sterilization Write short notes on THREE of the following conditions: Antepartum haemorrhage Hypertension in pregnancy Management of a woman with hyperemesis gravidarum at 8 weeks amenorrhoea Induction of labour Antepartum haemorrhage Def: bleed from genital tract after period of viability (28 weeks but slowly shifting to 24/52) Incidence: 5% of all preg Major causes: Placenta previa, Apruptio placenta. Minor causes: vasa previa, cervicitis, trauma, tumours, infxn, polyps, varicosities Hx Initiation factors- trauma, coitus Amt n nature Ass abdo pain/ uterine contractions Prev PV bleed/ ruptured membranes Gestational age Placental site based on prev U/S scan PE Mum Vitals, shock? Abdo: uterus=dates? Tenderness, contractions No VE unless excluded previa Fetus: fetal distress? Mx Immediate IV fluids Invx: FBC, GXM, Coagulation profile, U/E/Cr U/S Long term Previa: long term hospitalization, serial U/S, decide mode of del at 37 weeks Abruptio: short term hosp till stablised, monitor fetal growth, elective del at term Hypertension in pregnancy Def: hypertension 1st detected after 20/52 preg or rise of 30/15 mmHg over baseline if already hypertensive Inc: 7% Hypertensive conditions in preg 1) PIH-non proteinuric -pre eclampsia -eclampsia 2) Superimposed PIH 3) Chronic HT 4) HELLP PIH Risk factors: primate, >35 years old, preexisting HT, renal, autoimmune dz, multiple gestation, prev PIH, mother who had PIH, molar preg Cx: Maternal- eclapmsia, CVA, renal, hepatic, heart failure, pul edema, coag disturbances, abruption Fetus- acute hypoxia leading to IUD, distress or chronic hypoxia leading to IUGR MX 1) Admit 2) Assess severity Clinical- sympt of IE, BP, tendon reflexex 4 hourly Invx- 24h urine output, UTP, CCT, FBC, LFT, coag screen 3) Control BP acute- IV hydralazine, labetalol chronic- methyldopa, nifedipine, labetalol 4) Monitor mum Clinically- sympt, BP, urine output, reflexes Invx- 24h urine output, UTP, CCT, FBC, LFT, coag screen 5) Monitor baby growth-SFH, U/S hypoxia- FM, liquor, CTG, doppler, AFI 6) Deliver at 37/52 9earlier if IE, low plt, deranged LFT, dec AFI, abn CTG route vaginal unless very preterm, cervix unfav, malpresentation Management of a woman with hyperemesis gravidarum at 8 weeks amenorrhoea Def: intractable nausea vomiting Inc: 1% Pred factors: primips, youth, non smokers, multiple gestation, molar Hx: vomiting and inability to retain food PE: wt loss, signs of dehydration and hypovolemia Invx: electrolyte imbalances: hypoNa, hypoK, hypo Cl alkalosis urine for ketonuria and input output chart bld for acetone renal, hepatic function U/S (molar, twins) To rule out GE, cholecystitis, pancreatitis, PUD b4 treatment Mx Immed if severe Admit Parenteral antiemetics (metoclopramide) Enteral feeding Monitor glucose Hydration Counselling If non severe, symp[tomatic treatment Prevent vomiting by taking smaller meals, sitting upright after meals, sleep propped up Medications: antacids, H2 blockers, PPI Induction of labour Def: Artificial termination of pregnancy anytime after 28th week by a method that aims to secures vaginal delivery Inc: 10% Ind: Maternal- Hypertension/PE, DM Fetal- Rhesus dz, abruption, IUD, post term Placental- insufficiency Contraind: ( similar to NVD) Absolute- PPmajor, >2 prev LSCS, cerclage, maternal dz, CPD, non longitudinal lie, cord presentation, fetal distress Relative- grand multip, uterine scar, footling, premature Method: Cervical priming with Prostin pessary(up to 4) if mod Bishops score <5 Acute rupture of membranes/ amniotomy Oxytocin after ARM Start with 2.5 units in 500ml saline escalate dose every 30 min till optimum painful contractions and labour established. STOP if signs of hyperstimulation(>6 contractions in 10min) or CTG abn Cx: ARM chrioamnionitis, cord prolapse, abruption, amniotic fluid embolism Oxytoxin- failed induction, fetal distress, uterine rupture, hyperstimulation, hyponatremia, PPH(atony) A 38-year-old woman is married to her 39-year-old husband for the last 8 years and not been able to conceive in spite of not using any form of contraception. Discuss the management of this couple with primary subfertility Primary infertility is the term used to describe a couple that has never been able to conceive a pregnancy, after at least 1 year of unprotected intercourse. The term secondary infertility describes couples who have previously been pregnant at least once, but have not been able to achieve another pregnancy. Hx Female Menstrual History: Regular periods? (ovulating) Dysmenorrhea? (endometriosis) Menorrhagia? (fibroids)Male Past medical history: diabetes, salfasalazin, orchitis, alpha reductase inhibitor intake Surg probs: hernia op, torsion testes Social: smoker/drinker?Sex Erection? Ejeculation (intra vaginal)? FrequencyRelevant past med history Eg: PID Inx Female: Hormonal profile (1st 3 day 3 of menses) FSH LH PRL TSH Mid luteal progesterone U/S pelvis HSG/ laparoscopy, hydrotubation, hysteroscopyMale: HSA Number, structure, motility Mx If LH 2-3X FSH suspect PCOS (hirsute, obese, acne) Give Clomiphene citrate for 6months if ovulating Give gonadotrophins (super ovulation intrauterine injection) x 3 cycles ART (IVF etc) (refer to 2001, Q6b) A 30-year-old single woman, planning to get married the following month, attended a gynaecological clinic for routine Pap Smear. On examination, she was found to have a 10-cm left ovarian cyst. Discuss the management of this woman who is asymptomatic. Intro Diff diagnosis 1) Functional -Follicular (follicle fails to rupture; regresses in next menstrual cycle) - Lutein cyst (corpus lutein becomes haemorrhagic/cystic; larger, firmer, causes pain, may alter menstrual cycle) 2) Neoplastic -Epithelial (serous; mucinous) - Stromal (gynandroblastomas; granulosa-theca cell; sertoli-leydig cell) - Germ cell (teratoma) 3) Metaplastic- endometriosis 4) Inflammatory- Neisserian/pyogenic/granulomatous salphingo-oophoritis History Menstrual history- regularity; dysmenorrhoea (endometriosis); IMB/PCB? Other probs- abd pain? Abd distention? Vaginal d/c? bowel/bladder disturbances? LOW? LOA? Past med history- other CAs before, i.e: breast, colon. Family history- ovarian CAs, gynae probs. P/E Pelvic mass-fixed, solid, irregular? Ascites? Bimanual palpation- adenexa palpable? Mobile/ fixed/ mass in pouch of Douglas? Complications 1) Functional cysts- torsion - infarction - rupture - hemoperitoneuem (risk increases >5cm) - CA? 2) Neoplastic - malignant - malignant potential - pseudomyxoma peritonei (mucinous tumour with benign peritoneal implants on bowel surface) - mucocele of appendix (mucinous tumour) - functioning tumours (GT ! feminizing; SL ! virilizing) 3) Endometriosis- dysmenorrhoea - dyspareunia - dyschezia - infertility - torsion, infarction, rupture, haemorrhage - malignant change Investigations 1) U/S (day 2-5 of next menstrual cycle) regress? solid vs cystic; uniloculated vs multiloculated; scoring system for malignant potential- >7; ascites? 2) CA 125; CEA 3) Laparotomy/scopy for histology Guidelines on treatment 1) Functional cysts in reproductive years ! <6cm ! wait for next menstrual cycle to see if regresses ! 6-8cm; fixed solid ! ultrasound  unilocular multilocular - leave alone - cystectomy 2) Neoplastic in reproductive years - epithelial ! ovarian cystectomy with preservation of ovary - stromal-cell in reproductive years ! salpingo-oophorectomy - germ-cell ! cystectomy 3) Endometriosis in reproductive years ! pain relief ! NSAIDS ! surgery ! cystectomy and clearance of lesions ! hormonal manipulation ! OCP until want to get pregnant ! try for child ! naturally ! IVF 4) Malignant tumour- Surgical staging at laparotomy - consider unilat salphingo-oopherectomy (conservative) if Stage 1A, compliant with F/U, non high grade tumour. Once completed family- THBSO +/- chemo Write short notes on THREE of the following: Tubal ectopic pregnancy Cervical intra-epithelial neoplasia (CIN) Problems associated with the intra-uterine contraceptive device Management of recurrent vaginal discharge Tubal Ectopic pregnancy Ectopic pregnancies have a prevalence of 22 per 1000 live births. 95-98% are tubal in nature. OF these 50% occur in the ampulla, 20% in the isthmus, 12% fimbrial and 10%interstitial. They occur when implantation of the fertilized egg takes place in a site of the tube which offers an area for placentation. The extravillous trophoblast penetrates the full thickness of the tubal wall and due to the limited distensibility of the tube, the tube will eventually rupture. Although usually causing fetal death and maternal instability, the fetus sometimes maintains its circulation and a secondary abdominal pregnancy develops. Risk factors include previous ectopic pregnancies, increased maternal age, increased number of sex partners, IUD usage and PID. Rate of ectopic pregnancy in women with previous known PID is increased 6-10 times higher than in women with no previous history of PID. Tubal sterilization is also a risk factor. After non-laparoscopic tubal ligation about 12% of pregnancies are ectopic. After laparoscopic tubal coagulation about 51% of pregnancies are ectopic. Fertility treatment is also linked with ectopic implantation. Ovulation induction with clomiphene citrate or injectable gonadotropin therapy has been linked with a 4-fold increase in the risk of ectopic pregnancy in a case-control study. About 2-5% of clinical pregnancies are ectopic with IVF. The administration of hormones, specifically estrogen and progesterone, can slow the normal movement of the fertilized egg through the tubal epithelium and result in implantation in the tube. Women who become pregnant despite using progesterone-only oral contraceptives have a 5-fold increase in the ectopic pregnancy rate. They usually present with per vaginal bleeding, oftentimes passing old blood, iliac fossa pain, cramping unilaterally and amenorrhea. A ruptured ectopic pregnancy can present with sharp lower abdominal and shoulder pain, and vascular instability. On physical examination, 50% have a palpable adnexal mass, and 75% may have abdominal tenderness. Approximately 20% of patients with ectopic pregnancies are hemodynamically compromised at initial presentation, which is highly suggestive of rupture. A proper history and physical examination with a high index of suspicion is required for diagnosis. Important laboratory investigations include urine pregnancy test and determination of the serum progesterone level and serum quantitative -hCG levels. Ultrosonography is used to visualize the presence of extrauterine gestational sacs. If not visualized, the HCG levels can be used in conjunction. A HCG level of 6000iU/L and 1500iU/L should indicate an ability to visualize an intrauterine gestation sac via trans abdominal and transvaginal ultrasound respectively. Inability to do so suggests the presence of an ectopic pregnancy. Surgical treatment involves either performing a salpingectomy or salpingostomy via either laprotomy or laproscpy. Currently, laparotomy is the preferred technique when the patient is hemodynamically unstable, the surgeon has not been trained in laparoscopy, physical facilities and supplies to perform laparoscopic surgery are lacking or technical barriers to laparoscopy are present. Salpingectomy is used much less often than salpingostomy. It is preferred only in patients with uncontrolled bleeding, extensive tubal damage or recurrent ectopic pregnancy in the same tube. Medical treatments involves the puncture and aspiration of the gestational sac using prostaglandins, methotrexate or KCl. indications include hemodynamic stability, significant risk associated with general anesthesia, patient compliance, lack of contraindications to methotrexate therapy, small size of ectopic mass and lack of fetal cardiac motion.  HYPERLINK "http://www.aafp.org/afp/20000215/1080.html" http://www.aafp.org/afp/20000215/1080.html CIN CIN is the dysplasia of the epithelial layer of the cervix. It usually occurs at the squamo-columnar junction in the cervix which is the transformation zone of the epithelium between the endocervix and ectocervix. It is classified depending on the extent to which the epithelium is affected. Mild dysplasia tends to affect only the deepest third of the epithelium. Moderate dysplasia affects 2/3rds and severe showing dysplasia across the full thickness of the epithelium. CIN is a true precursor of squamous cell carcinoma and more than 50% of untreated CIN 3 will progress to invasive cancer in 15-25 years. Risk factors for the development of CIN and eventually cervical cancer include HPV infection, early sexual debut, smoking, multiparity and OCP usage. HPV infection in particular has a 99.7% etiological relationship. The initial investigation associated with diagnosis of CIN is the pap smear. The severity of dyskariosis is related to the level of CIN. Abnormal pap smears suggestive of CIN II and III are reason to undergo colposcopy with locates the lesion on the cervix, indicted severity of the intra epithelial neoplasia and allows selection of sites of the lesion for biopsy. Smears suggestive of mild dyskariosis will have a repeat smear during follow up. Treatment of CIN involves both ablative as well as excision therapies. Ablative therapies include hot cautery, electrocoagulation diathermy, cold coagulation, cryotherapy and laser ablation. Excision therapies include large loop excision of the transformation zone, laser cone biopsies and knife cone biopsies. These are potentially curative measures if the margins of excision are found to be clear. Problems associated with IUCD use. IUCDs are generally very reliable contraceptive devices but do come with a host of problems. They include perforation during insertion which is a rare event but requires surgical intervention to correct. Presence of an IUD also is associated with dysmenorrhea, heavy menstrual flow and an increased risk for PID. Compared to other contraceptive devices it does not offer any protection against STDs. Besides adverse effects from their use, complications associated with their use include a higher percentage of ectopic pregnancies compared to normal pregnancies even though there is an overall reduction in the number of pregnancies. In addition there is a small chance for conception to occur when the IUD is in place. In addition, the strings which are attached to the IUD can go missing which implies either that the IUCD has been expelled or that it has retracted into the uterine cavity. This scenario might even necessitate surgical removal. The introduction of hormone releasing IUDS, has helped to decrease the incidence of side effects such as dysmenorrhea and menorrhagia. However it has been noted to cause side effects like abdominal and breast pain as well as nausea. The management of recurrent vaginal discharge The management of recurrent discharge can be divided based on their etiologies. Physiological discharge is white and usually turns yellow on contact with air. It usually occurs mid cycle, in pregnancy and upon initiation of oral combined OCPs. Chief among the obstetric causes of vaginal discharge would be an ectopic pregnancy which usually causes a bloody discharge. Other causes would include threatened abortions as well as ante partum hemorrhage. Gynecological causes include those due to cervical and vaginal cancers which are typically blood stained discharges. The other major group involves those due to infections. Infections of the lower genital tract include a candida infection which causes a white curdy discharge which can also be thin and watery with a yeasty smell. Bacteral vaginosis causes a yellowish discharge which releases a fishy smell on addition of an alkali. Trichomoniases causes a greenish yellowish discharge. PIDs also are associated with discharges.    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In the history, the nature of the discharge is important, especially the timing, the type of discharge, its colour, smell and the presence of blood. Other significant histories include a complete menstrual history and questions to rule out pregnancy. A sexual history is required to check for the possibility of STDs and to check if the patients partner is similarly affected. The presence of constitutional symptoms of fever to suggest infections and loss of weight and appetite which suggest malignancy should also be taken. Physical examination, especially a speculum examination can help to reveal the source of the discharge as well as any lesions on the visible genital tract. Laboratory investigations include a full blood count to check for infections, a culture of the discharge and a high vaginal swab and an endocervial swab. Treatment is dependent of the cause and relevant therapy should be instituted as required. &1h:p$?. 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