Oesophageal atresia/TE fistula may be suspected prenatally with ultrasound findings of polyhydramnios, absence of fluid in the stomach, small sized abdomen, or the presence of a dilated proximal oesophageal pouch. An underlying disease is only found in 17 % of cases in mild polyhydramnios. In contrast, an underlying disease is detected in 91 % of cases in moderate to severe polyhydramnios. The literature lists the following potential aetiologies: fetal malformations and genetic anomalies (8–45 %), maternal diabetes mellitus (5–26 %), multiple pregnancies (8–10 %), fetal anaemia (1–11 %), other causes, e.g. viral infections, Bartter syndrome, neuromuscular disorders, maternal hypercalcemia. Viral infections which can lead to polyhydramnios include parvovirus B19, rubella, and cytomegalovirus. Other infections, e.g. toxoplasmosis and syphilis, can also cause polyhydramnios.

Vesicovaginal fistula (VVF) is a subtype of female urogenital fistula (UGF). VVF is an abnormal fistulous tract extending between the bladder and the vagina that allows the continuous involuntary discharge of urine into the vaginal vault. The uncontrolled leakage of urine into the vagina is the hallmark symptom of patients with UGFs. Patients may complain of urinary incontinence or an increase in vaginal discharge following pelvic surgery or pelvic radiotherapy with or without antecedent surgery. The drainage may be continuous; however, in the presence of a very small UGF, it may be intermittent. Increased postoperative abdominal, pelvic, or flank pain; prolonged ileus; and fever should alert the physician to possible urinoma or urine ascites and mandates expeditious evaluation. Recurrent cystitis or pyelonephritis, abnormal urinary stream, and haematuria also should initiate a workup for UGF.

Urinary trace infection presents with dysuria and urgency.
Detrusor instability causes urge incontinence.
Neurogenic bladder from diabetic neuropathy would also have urgency.

Gestational trophoblastic disorder is characterized by an abnormal trophoblastic proliferation and include a complete and partial mole. It is characterized by persistently elevated BHCG levels after pregnancy and on ultrasound a snow storm appearance. These appear as anechoic areas on ultrasound.

The pelvic outlet is bounded anteriorly by the inferior border of the pubic arch, posteriorly by the sacrotuberous ligament and the tip of the coccyx and laterally by the ischial tuberosities.

If a cervical screening test reveals invasive squamous cell carcinoma or adenocarcinoma, refer the patient to a gynaecologist at a tertiary hospital right once for further treatment.
Colposcopy at a GP practice is not appropriate in these situations. When it comes to the prospect of cancer, reassurance isn’t enough.

This woman has signs and symptoms suggestive of cervical insufficiency, whose clinical features include pelvic pressure, premenstrual-like cramping and backache with increased vaginal discharge. Usually these symptoms will persist for several days to weeks.
Cervical insufficiency is seen between 14 – 20 weeks of gestation, which is presented as soft effaced cervix, with minimal dilation on physical examination and a 4 cm dilated and more than 80% effaced cervix will be the clinical presentation in a more advanced case.

Placental abruption presents with painful vaginal bleeding, whereas Placenta Previa presents as painless vaginal bleeding. Both cases will lead to shock but will not show any features of cervical insufficiency.

Anaemia, polyhydramnios, large for gestational age uterus and severe hyperemesis gravidarum are the commonly associated symptoms of a twin pregnancies.

New menstrual cycle after an abortion is expected to be presented with cervical dilation however signs of effacement will not be present along with it.

The occurrence of migraine in women is influenced by hormonal changes throughout the lifecycle. A beneficial effect of pregnancy on migraine, mainly during the last 2 trimesters, has been observed in 55 to 90% of women who are pregnant, irrespective of the type of migraine.

For treatment of acute migraine attacks, 1000 mg of paracetamol (acetaminophen) preferably as a suppository is considered the first choice drug treatment. The risks associated with use of aspirin (acetylsalicylic acid) and ibuprofen are considered to be small when the agents are taken episodically and if they are avoided during the last trimester of pregnancy.

Paracetamol 500 mg alone or in combination with metoclopramide 10 mg are recommended as first choice symptomatic treatment of a moderate-to-severe primary headache during pregnancy.

Yasmin has been linked to decreased fluid retention and weight gain as a side effect of COCs, which is why most women who experience this side effect prefer Yasmin®.
Due to its anti-mineralocorticoid properties, drospirenone, unlike earlier progestogens, is associated with no weight gain or even moderate weight loss.
Yasmin has a similar failure rate to other COCs. No evidence using Yasmin is linked to a lower risk of cervical cancer as a long-term side effect of COCs. Yasmin, like all COCs, can cause spotting and irregular bleeding in the first few months of use.
Drospirenone, a progesterone component, has antiandrogenic properties and is slightly more successful in treating acne, but the difference is not big enough to make it preferable in terms of acne therapy or prevention when compared to other COCs.

Asherman syndrome (intrauterine adhesions or intrauterine synechiae) occurs when scar tissue forms inside the uterus and/or the cervix. These adhesions occur after surgery of the uterus or after a dilatation and curettage.

Patients with Asherman syndrome may have light or absent menstrual periods (amenorrhea). Some have normal periods based on the surface area of the cavity that is affected. Others have no periods but have severe dysmenorrhea (pain with menstruation).

Although two-dimensional sonography may suggest adhesive disease, Asherman syndrome is more often evaluated initially with saline sonography or hysterosalpingography to demonstrate the adhesions.

Her most likely diagnosis would be an ovarian carcinoma. Any palpable adnexal mass in a post-menopausal woman is a red flag for an ovarian malignancy and should be assumed so until proven otherwise.

Endometrial cancer typically presents with a post-menopausal bleed and although there might be uterine enlargement, an adnexal mass is generally absent.

It is very rare for follicular cysts to develop following menopause and it is uncommon for post-menopausal women to have a benign ovarian tumour, which is more common in younger women. A degenerating leiomyoma would be unlikely in this case, especially since her pelvic examination three years ago was normal (no history of leiomyoma noted).

The most common cause of maternal mortality is Cardiovascular deaths due to post partum bleeding followed by hypertensive disorders of pregnancy, sepsis and complications of labour.

6 and 11 are considered low risk and are commonly associated with genital warts and low-grade squamous intraepithelial lesions of the cervix (can correspond cytologically to CIN 1)

Intrahepatic cholestasis of pregnancy can affect both mother and foetus, however it is more harmful for the foetus. Amongst foetuses, there is an increased risk of perinatal mortality, meconium aspiration, premature delivery and post partum haemorrhage. Exact cause of fetal death cannot be predicted accurately but it is not related to intra uterine growth retardation or placental insufficiency. The liver can be affected in the mother leading to generalized pruritis but no evidence of fetal hepatic dysfunction has been found.

Oxytocin binds to the G protein coupled receptors that triggers the IP3 mechanism leading to an elevated intracellular calcium ion.

Endometrioid endometrial carcinoma is oestrogen-responsive, and the main risk factor for this disease is long-term exposure to excess endogenous or exogenous oestrogen without adequate opposition by a progestin.

Early age at menarche is a risk factor for endometrial carcinoma in some studies; late menopause is less consistently associated with an increased risk of the disease. Both of these factors result in prolonged oestrogen stimulation and at times of the reproductive years during which anovulatory cycles are common

Other risk factors include
obesity,
nulliparity,
diabetes mellitus, and
hypertension.

The risk of endometrial hyperplasia and carcinoma with oestrogen therapy can be significantly reduced by the concomitant administration of a progestin. In general, combined oestrogen-progestin preparations do not increase the risk of endometrial hyperplasia.

Endometrial carcinoma usually occurs in postmenopausal women (mean age at diagnosis is 62 years). Women under age 50 who develop endometrial cancer often have risk factors such as obesity or chronic anovulation.

Treatment for infertility caused by ovulation issues has had the best results by far. PCOS, also known as Stein-Leventhal syndrome, is marked by hyperandrogenism, tiny cysts in the ovaries, acne, and hirsutism, as well as ovulation issues that result in anovulatory cycles due to hormonal imbalance.

70% of females with anovulatory periods begin ovulation under medical supervision, and 50% of those conceive within 6 to 9 months.

Infertility can be caused by low or no sperm counts, poor sperm motility, or dysmorphic sperms. Treatment options include fertility medicines that promote sperm production, artificial insemination with donor sperm, and intracytoplasmic injection of sperm, but success rates are poor (less than 25 percent ). Following pelvic inflammatory disease, previous surgery, or tuberculosis, the Fallopian tubes become obstructed or damaged, preventing sperm from reaching the ovum. Tubal blockages and adhesions are treated by laparoscopic surgery. The success rate of conception varies greatly depending on the degree of the blockage, ranging from 10% to 70%.

Turner syndrome is linked to infertility and ovarian dysgenesis. Treatment for gonadal dysgenesis and reversal of infertility is not an option. Because of the high likelihood of miscarriages, even after egg donation, the success rate is relatively low.

In Cushing’s syndrome there is excess cortisol. Causes are broadly divided into 2 types: ACTH dependent disease: excess ACTH from the pituitary (Cushing’s disease), ectopic ACTH-producing tumours or excess ACTH administration. Non-ACTH-dependent: adrenal adenomas, adrenal carcinomas, excess glucocorticoid administration. The recommended diagnostic tests for the presence of Cushing’s syndrome are 24-hour urinary free cortisol, 1 mg overnight dexamethasone suppression test and late-night salivary cortisol. There are several other tests that may also be performed to find the cause. ACTH and cortisol measured together may show if this is ACTH dependent or not. MRI pituitary and CT abdo and pelvis may show if tumour is the cause.

Among all the antiepileptic drugs sodium valproate carries the highest teratogenicity rate. The potential congenital defects caused by sodium valproate are as below:
– Neural tube defects like spina bifida, anencephaly
– Cardiac complications like congenital ventricular septal defect, aortic stenosis, patent ductus arteriosus, aberrant pulmonary artery
– Limb defects like polydactyly were more than 5 fingers are present, oligodactyly were less than 5 fingers are present, absent fingers, overlapping toes, camptodactyly which is presented as a fixed flexion deformity of one or more proximal interphalangeal joints,split hand, ulnar or tibial hypoplasia.
– Genitourinary defects like hypospadias, renal hypoplasia, hydronephrosis, duplication of calyceal system.
– Brain anomalies like hydranencephaly, porencephaly, arachnoid cysts, cerebral atrophy, partial agenesis of corpus callosum, agenesis of septum pellucidum, lissencephaly of  medial sides of occipital lobes, Dandy-Walker anomaly
– Eye anomalies like bilateral congenital cataract, optic nerve hypoplasia, tear duct anomalies, microphthalmia, bilateral iris defects, corneal opacities.
– Respiratory tract defects like tracheomalacia, lung hypoplasia,severe laryngeal hypoplasia, abnormal lobulation of the right lung, right oligemic lung which is presented with less blood flow.
– Abdominal wall defects like omphalocele
– Skin abnormalities capillary hemangioma, aplasia cutis congenital of the scalp.

Turner syndrome patients present with primary amenorrhea, have non functional or streak ovaries and cant conceive. They are 45X genetically.

Sertoli cells contain receptors for FSH. In response to this Sertoli cells synthesize inhibin, androgen binding proteins and anti Mullerian hormone all which are connected to the reproduction cycle.

The biochemical and mechanical effects of progesterone and the enlarging uterus are responsible for some changes in lung function during pregnancy.

Progesterone increases the sensitivity of the respiratory centre to arterial carbon dioxide while also causing hyperaemia in the airway leading to nasal obstruction. As a result, minute ventilation and tidal volume increase by 50% to allow greater arterial oxygen saturation.

The enlarging uterus displaces the diaphragm upwards, and also limits the movement of the thoracic cage, thereby decreasing the functional residual capacity (FRC) and the expiratory reserve volume (ERV) by 20%.

Functional Expiratory Volume in 1 second (FEV1) and Forced Vital Capacity (FVC) remain unchanged in pregnancy.

During the ovulatory cycle, only one follicle will ovulate. The remaining non-ovulating follicles undergo disintegration. This process is known as atresia.

The basic components of the mammary gland are the alveoli. These are lined with milk-secreting cuboidal cells surrounded by myoepithelial cells. The alveoli join to form groups known as lobules. The lobules form lobes. Each lobe has a lactiferous duct that drains into openings in the nipple. Each breast typically contains 15-20 lobes.

After the release of the oocyte, the theca and the granulosa cells form the corpus luteum which undergoes extensive vascularization for continued steroidogenesis. Progesterone is secreted by the luteal cells and is synthesized from cholesterol.

Involution of the uterus takes 4-6 weeks

This patient presenting with oligohydramnios in her third trimester and had reported an episode of sudden gush of fluid secondary to ruptured membrane which she had mistaken to be “urinary incontinence”.  Hence, the most likely cause of oligohydramnios in this patient will be premature preterm rupture of membrane (PPROM).

An amniotic fluid volume which is less than expected for gestational age is called as Oligohydramnios and is typically diagnosed by ultrasound examination. This condition can be qualitatively described as reduced amniotic fluid volume and quantitatively as amniotic fluid index ≤5 cm or a single deepest pocket <2 cm. Oligohydramnios either can be idiopathic or may have a maternal, fetal or placental cause. Fetal prognosis in this case depends on several factors like the underlying cause, the severity of loss ie. reduced versus no amniotic fluid state and the gestational age at which oligohydramnios occurred. As an adequate volume of amniotic fluid is critical for the normal fetal movements, for fetal lung development and for cushioning the fetus and umbilical cord from uterine compression, so pregnancies complicated with oligohydramnios are at higher risk for fetal deformation, pulmonary hypoplasia and umbilical cord compression.
Oligohydramnios is also associated with an increased risk for fetal or neonatal death, which can either be related to the underlying cause of reduction in amniotic fluid volume or due to the sequelae caused due to reduced amniotic fluid volume. The amniotic fluid volume reflects the balance between fluid production and movement of fluid out of the amniotic sac and the most common mechanisms behind oligohydramnios are fetal oliguria/anuria or fluid loss due to rupture of membranes; also reduction in the amount of lung fluid or increased swallowing do not play major roles in this. Idiopathic cases as in idiopathic oligohydramnios, may be due to alterations in the expression of water pores like aquaporin 1 and aquaporin 3, present in fetal membranes and placenta.

Causes of oligohydramnios
a) Maternal causes includes:
– Medical or obstetric conditions associated with uteroplacental insufficiency like preeclampsia, chronic hypertension, collagen vascular disease, nephropathy, thrombophilia.
– Intake of medications like angiotensin converting enzyme inhibitors, prostaglandin synthetase inhibitors, trastuzumab.
b) Placental causes are:
– Abruption of placenta
– Twin polyhydramnios-oligohydramnios sequence which is the Twin to twin transfusion
– Placental thrombosis or infarction
c) Fetal cases leading to oligohydramnios are:
– Chromosomal abnormalities
– Congenital abnormalities which are associated with impaired urine production
– Growth restriction
– Demise
– Post-term pregnancy
– Ruptured fetal membranes
– Infections
– Idiopathic causes

During First trimester: Etiology of oligohydramnios during the first trimester is often unclear. As the gestational sac fluid is primarily derived from the fetal surface of the placenta via transamniotic flow from the maternal compartment and secretions from the surface of the body of the embryo reduced amniotic fluid prior to 10 weeks of gestation is rare.

During Second trimester: Fetal urine begins to enter the amniotic sac and fetus begins to swallow amniotic fluid by the beginning of second trimester, therefore, during this period any disorders related to the renal/urinary system of the fetus begins to play a prominent role in the etiology of oligohydramnios. Some of such anomalies include intrinsic renal disorders like cystic renal disease and obstructive lesions of the lower urinary tract like posterior urethral valves or urethral atresia. Other common causes of oligohydramnios in the second trimester are maternal and placental factors and traumatic or nontraumatic rupture of the fetal membranes.

During Third trimester: Oligohydramnios which is first diagnosed in the third trimester is often associated with PPROM or with conditions such as preeclampsia or other maternal vascular diseases leading to uteroplacental insufficiency. Oligohydramnios frequently accompanies fetal growth restriction as a result of uteroplacental insufficiency.

Under the influence of prolactin, oestrogen and progesterone and human placental lactogen (hPL), the mammary epithelium proliferates but remains presecretory during mammogenesis. Lactogenesis is inhibited by high circulating levels of progesterone and oestrogen which block cortisol binding sites. Cortisol would have otherwise have worked synergistically with prolactin in milk production. A sharp decrease in progesterone levels after delivery allows prolactin and oxytocin to stimulate milk production and the milk ejection reflex in response to suckling. Prolactin continues to maintain milk production in galactopoiesis.

This patient had postmenopausal vaginal haemorrhage and an 8mm endometrial thickness. Endometrial thickness of 4mm or more in a postmenopausal woman with vaginal bleeding necessitates an endometrial biopsy to rule out endometrial cancer, and this patient should be referred to a gynaecologist for this procedure.
All of the other choices are incorrect.

Both the female hormones, namely progesterone and oestrogen as well as the male hormones or androgens are lipid soluble. The common precursor of these is cholesterol.

If the patient has a negative Chlamydia screen then a stat dose of metronidazole monotherapy is appropriate. You do not know this patients Chlamydia status and therefore dual therapy with metronidazole + doxycycline or azithromycin is appropriate.