This patient has a regular and long menstrual period. The most crucial thing in this case is to rule out anovulation.
Serum progesterone concentration is the best test for detecting ovulation.
Ovulation has occurred if the level is greater than 20nmol/L.
This test should be performed 3 to 10 days prior to the start of the next anticipated period.

The given case where the patient presents with sudden abdominal pain, cessation of uterine contraction and the urge to push along with vaginal bleeding is typical for uterine rupture. Examination shows a decreased or lost fetal heart rate, along with signs of fluid collection including fluid thrill and shifting dullness due to the entry of blood into the peritoneal cavity.
Other common manifestations of uterine rupture include:
– Loss of the station of the fetal presenting part
– Vaginal bleeding which is not be proportionate to the hemodynamic status
-Maternal tachycardia and hypotension ranging from subtle to severer shock
– Uterine tenderness
– Change in uterine shape and contour
– Easily palpable fetal parts
– No fetal presentation on vaginal examination
– Hematuria if the rupture extends to the bladder
Anterior lower transverse segment is the most common site of spontaneous uterine rupture.

Placenta previa usually presents as painless vaginal bleeding, which rules it out as the diagnosis in given case.

Vaginal bleeding with a tender and tense uterus is the presentation in placental abruption, also contrary to uterine rupture, uterine contractions will continue in case of placental abruption.

Cervical laceration can be a possibility, but in such cases more amount of vaginal blood loss was expected in this patient with hemodynamic instability. Also symptoms like deformed uterus, abdominal distention and cessation of contractions are inconsistent with cervical laceration.

Excessive generation of thrombin and fibrin in the circulating blood results in Disseminated intravascular coagulation (DIC) which leads to increased platelets aggregation and consumption of coagulation factors resulting in consequent bleeding at one site and thromboembolism at another. Placental abruption and retained products of conception in the uterine cavity are the most common obstetric causes of DIC. The condition will not fit as diagnosis in this clinical scenario.

The risk of developing endometrial carcinoma is less than 5% over 20 years if the endometrium shows hyperplasia without atypia.
There are 2 types of Endometrial Hyperplasia:
1. Hyperplasia without atypia*
2. Atypical hyperplasia

Major Risk Factors:
Oestrogen (HRT)
Tamoxifen
PCOS
Obesity
Immunosuppression (transplant)

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.

Although uterine growth during the first few weeks of pregnancy is accomplished by increased numbers of smooth muscle cells (i.e. hyperplasia) and a smaller contribution from increased cell size (i.e. hypertrophy), the predominant growth of the uterus during pregnancy is by way of stretch‐induced myometrial hypertrophy. This ongoing process of stretch‐induced tissue remodelling and smooth muscle hypertrophy is accompanied by the lack of uterine contractions during most of gestation to accommodate the developing foetus (phase 0 of parturition). Phase 1 of parturition represents myometrial activation. The final stages of pregnancy are characterized by increases in spontaneous low‐amplitude contractions that gradually increase in frequency, rhythmicity and strength, normally culminating in labour and delivery of the foetus at term (phase 2 of parturition).

It is stage 2 of the disease.

Staging:
1 Confined to uterus
1A < 50% myometrial invasion
1B > 50% myometrial invasion
2 Cervical stromal invasion but not beyond uterus
3 Extension beyond the uterus
3A Tumour invades the serosa or adnexa
3B Vaginal and/or parametrial invasion
3C1 Pelvic nodal involvement
3C2 Para aortic nodal involvement
4 Distant Metastasis
4A Tumour invasion of the bladder and/or bowel mucosa
4B Distant metastases including abdominal metastases and/or inguinal lymph nodes

Chlamydia is one of the most prevalent STIs in the UK. Many infected individuals can be asymptomatic making it difficult to detect. The gold standard in the diagnosis of Chlamydia is the nucleic acid amplification test (NAAT). A sample is taken from a vulvovaginal self swab, or a cervical swab on speculum examination in women.

There is 70% chance that a women who has had a C-section can deliver via spontaneous vaginal delivery.

The Rotterdam criteria was developed and expanded by the European Society of Human Reproduction and Embryology/American Society for Reproductive Medicine Rotterdam consensus (ESHRE/ASRM) in 2003 and is now the Gold standard in the diagnosis of PCOS. The criteria requires two of three features: anovulation, hyperandrogenism, and polycystic ovaries seen on ultrasound.

The National Institute of Child Health and Human Development (NICHD) attempted to define PCOS in 1990 but omitted ultrasonographic evidence of polycystic ovaries which is considered to be diagnostic of PCOS.

The Androgen Excess Society (AES) served to confirm hyperandrogenism as the central event in the development of PCOS.

The ROME III criteria is used for Irritable Bowel Disease and is therefore not applicable to PCOS.

The Australasian Diabetes in Pregnancy Society recommends a 50 or 75 g glucose challenge at 26–28 weeks in all pregnant women. An OGTT should be performed if the test result is abnormal: 1 hour values after a 50 or 75 g glucose challenge exceeding 7.8 or 8.0 mmol/L respectively.

If a woman has had gestational diabetes, a repeat OGTT is recommended at 6–8 weeks and 12 weeks after delivery. If the results are normal, repeat testing is recommended between 1 and 3 years depending on the clinical circumstances.

Cholestasis of pregnancy is associated with increased fetal morbidity and mortality and should be treated actively. The significance attached to pruritus in pregnancy is often minimal, but it is a cardinal symptom of cholestasis of pregnancy, which may have no other clinical features.

Elements of the Apgar score include colour, heart rate, reflexes, muscle tone, and respiration. Apgar scoring is designed to assess for signs of hemodynamic compromise such as cyanosis, hypoperfusion, bradycardia, hypotonia, respiratory depression or apnoea. Each element is scored 0 (zero), 1, or 2. The score is recorded at 1 minute and 5 minutes in all infants with expanded recording at 5-minute intervals for infants who score 7 or less at 5 minutes, and in those requiring resuscitation as a method for monitoring response. Scores of 7 to 10 are considered reassuring.

Prostaglandin E1 and E2 help maintain the patency of the DA during pregnancy. PGE2 is by far the most potent and important. It is produced in large quantities by the placenta and the DA itself.

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.

In pregnancy, progesterone is produced by the corpus luteum followed by the placenta- Exogenous progesterone will not lead to withdrawal bleeding. In ovarian failure as well as pituitary failure, no oestrogen stimulation of the endometrium exists, and progesterone cannot cause withdrawal bleeding. With Mullerian agenesis, there is no endometrium. Polycystic ovarian syndrome has an abundance of circulating oestrogen, so the endometrium will proliferate.

→ In pregnancy progesterone withdrawal will not occur since the corpus luteum is producing progesterone- The placenta will take over, starting at 7 weeks, and will be the sole producer of progesterone by 12 weeks.
→ In ovarian failure no oestrogen will be produced; no proliferation of the endometrium will occur.
→ Pituitary failure is an incorrect answer because without gonadotropin stimulation, there will not be enough oestrogen to stimulate the endometrial lining.
→ Mullerian agenesis is an incorrect answer – there is no uterus, thus no bleeding.

Acute fatty liver of pregnancy occurs in 1-10000 pregnancies and presents as jaundice with abdominal pain. The maternal mortality is around 20%

Vaginal atrophy (thinning of vaginal tissue): Oestrogen helps to keep this tissue healthy. After menopause, low oestrogen levels can cause your vaginal walls to become thin, dry, and inflamed. That often leads to bleeding after sex.

Vaginal atrophy is the most common cause of post menopausal vaginal bleeding.

With a normal pap smear a year ago, this patient is unlikely to develop cervical cancer.

Cervical ectropions are not common in post-menopausal women.

Endometrial cancer and cervical polyps are possible causes of postcoital bleeding, however, they are not as common as vaginal atrophy.

This patient experiences a stress based mixed urinary incontinence presented as leakage of urine while sneezing or coughing and urgency which is an intense urge to urinate with small voiding volume as her symptoms. Urinary incontinence is common and may cause significant distress in some, as seen in this patient who wears a pad every day.  Initial evaluation of mixed incontinence includes maintaining a voiding diary, which helps to classify the predominant type of urinary incontinence and thereby to determine an optimal treatment by tracking the fluid intake, urine output and leaking episodes.

All patients with mixed incontinence generally require bladder training along with lifestyle changes like weight loss, smoking cessation, decreased alcohol and caffeine intake and practicing pelvic floor muscle exercises like Kegels. Depending on the predominant type, patients who have limited or incomplete symptom relief with bladder training may benefit from pharmacotherapy or surgery.

In patients with urgency-predominant incontinence, timed voiding practice like urinating on a fixed schedule rather than based on a sense of urgency along with oral antimuscarinics are found to be useful.

Surgery with a mid-urethral sling is performed in patients with stress-predominant incontinence which is due to a weakened pelvic floor muscles as in cystocele.

In patients with a suspected urethral diverticulum or vesicovaginal fistula, a cystoscopy is usually indicated but is not used in initial evaluation of urinary incontinence due to its cost and invasiveness.

Urodynamic testing involves measurement of bladder filling and emptying called as cystometry, urine flow, and pressure (eg, urethral leak point).  This testing is typically reserved for those patients with complicated urinary incontinence, who will not respond to treatment or to those who are considering surgical intervention.

Initial evaluation of mixed urinary incontinence is done by maintaining a voiding diary, which helps to classify predominant type of urinary incontinence into stress predominant or urgency predominant and thereby to determine the optimal treatment required like bladder training, surgical intervention, etc.

Pulmonary hypertension (PH) is an increase of blood pressure in the pulmonary artery, pulmonary vein, or pulmonary capillaries, leading to shortness of breath, dizziness, fainting, and other symptoms, all of which are exacerbated by exertion. PH in pregnancy carries a 25–56% maternal mortality rate with a mixture of intrapartum and postpartum deaths.

Current recommendations for management of PH in pregnancy include termination of pregnancy if diagnosed early, or utilizing a controlled interventional approach with early nebulized prostanoid therapy and early elective caesarean section under regional anaesthesia. Other recommended therapies for peripartum management of PH include sildenafil and nitric oxide.

Neural tube defects (NTDs) are common complex congenital malformations resulting from failure of the neural tube closure during embryogenesis. It is established that folic acid supplementation decreases the prevalence of NTDs, which has led to national public health policies regarding folic acid.

Neural tube defects (NTD) were 43% more common in Indigenous than in non-Indigenous infants in Western Australia in the 1980s, and there has been a fall in NTD overall in Western Australia since promotion of folate and voluntary fortification of food has occurred.

Women should take 5 mg/d of folic acid for the 2 months before conception and during the first trimester.

Women planning pregnancy might be exposed to medications with known antifolate activities affecting different parts of the folic acid metabolic cascade. A relatively large number of epidemiologic studies have shown an increased risk of NTDs among babies exposed in early gestation to antiepileptic drugs (carbamazepine, valproate, barbiturates), sulphonamides, or methotrexate. Hence, whenever women use these medications, or have used them near conception, they should take 5 mg/d of folic acid until the end of the first trimester of pregnancy.