Anaemia in pregnancy results from a greater increase in plasma volume compared to haemoglobin concentration, leading to a dilution of haemoglobin levels. It is important to note that haemoglobin levels actually increase during pregnancy. Drinking more water does not cause anaemia, as any excess water would be eliminated by the kidneys. Additionally, reduced secretion of ADH does not occur during pregnancy and would result in diuresis rather than anaemia.

During pregnancy, women are checked for anaemia twice – once at the initial booking visit (usually at 8-10 weeks) and again at 28 weeks. The National Institute for Health and Care Excellence (NICE) has set specific cut-off levels to determine if a woman requires oral iron therapy. For the first trimester, the cut-off is less than 110 g/L, for the second and third trimesters, it is less than 105 g/L, and for the postpartum period, it is less than 100 g/L. If a woman falls below these levels, she should receive oral ferrous sulfate or ferrous fumarate. Treatment should continue for three months after iron deficiency is corrected to allow for the replenishment of iron stores.

Adenomyosis is characterized by the presence of endometrial tissue within the myometrium, leading to symptoms such as heavy menstrual bleeding and painful periods. This can occur due to the separation of the endometrium from the myometrium, causing inflammation and discomfort. Ultrasound scans can detect an irregular myometrial border and a swollen uterus due to the accumulation of blood in the endometrial tissue. It is important to note that although adenomyosis and endometriosis share similar symptoms, they are distinct conditions that can coexist. Endometrial cancer is not a possible diagnosis as it does not involve the invasion of endometrial tissue into the myometrium.

Adenomyosis is a condition where the endometrial tissue is found within the myometrium. It is more commonly seen in women who have had multiple pregnancies and are nearing the end of their reproductive years. The condition is characterized by symptoms such as dysmenorrhoea, menorrhagia, and an enlarged, boggy uterus.

To diagnose adenomyosis, an MRI is the preferred investigation method. Treatment options include symptomatic management, tranexamic acid to manage menorrhagia, GnRH agonists, uterine artery embolisation, and hysterectomy, which is considered the definitive treatment.

During the early stages of pregnancy, the syncytiotrophoblast secretes hCG to prompt the corpus luteum to produce progesterone. This process typically begins around 6-7 days after fertilization and is complete by day 9-10. To ensure accurate results, it is recommended that women wait until at least the first day of their missed period to take a pregnancy test, as testing too early can result in a false-negative.

The role of hCG in pregnancy is crucial, as it stimulates the corpus luteum to produce progesterone, which is essential for maintaining a healthy pregnancy. In the first four weeks of pregnancy, hCG levels should double every 48-72 hours until they eventually plateau. Monitoring hCG levels through sequential blood tests can help identify potential issues such as miscarriage or ectopic pregnancy, as hCG levels may fall or plateau prematurely. It is important to note that hCG is not secreted by the blastocyst, corpus luteum, ovary, or zygote.

Endocrine Changes During Pregnancy

During pregnancy, there are several physiological changes that occur in the body, including endocrine changes. Progesterone, which is produced by the fallopian tubes during the first two weeks of pregnancy, stimulates the secretion of nutrients required by the zygote/blastocyst. At six weeks, the placenta takes over the production of progesterone, which inhibits uterine contractions by decreasing sensitivity to oxytocin and inhibiting the production of prostaglandins. Progesterone also stimulates the development of lobules and alveoli.

Oestrogen, specifically oestriol, is another major hormone produced during pregnancy. It stimulates the growth of the myometrium and the ductal system of the breasts. Prolactin, which increases during pregnancy, initiates and maintains milk secretion of the mammary gland. It is essential for the expression of the mammotropic effects of oestrogen and progesterone. However, oestrogen and progesterone directly antagonize the stimulating effects of prolactin on milk synthesis.

Human chorionic gonadotropin (hCG) is secreted by the syncitiotrophoblast and can be detected within nine days of pregnancy. It mimics LH, rescuing the corpus luteum from degenerating and ensuring early oestrogen and progesterone secretion. It also stimulates the production of relaxin and may inhibit contractions induced by oxytocin. Other hormones produced during pregnancy include relaxin, which suppresses myometrial contractions and relaxes the pelvic ligaments and pubic symphysis, and human placental lactogen (hPL), which has lactogenic actions and enhances protein metabolism while antagonizing insulin.

Schiller-Duval bodies seen on histology are a characteristic feature of yolk sac tumor, making it a pathognomonic finding.

1. Incorrect. Yolk sac tumor would not present with diffuse sheets, nests, and cords of large uniform tumor cells like testicular seminoma.

2. Incorrect. Call-Exner bodies are not present in yolk sac tumor.

3. Incorrect. Yolk sac tumor is not a metastasis from a diffuse-type gastric adenocarcinoma, which would have a signet cell histology appearance.

4. Incorrect. Yolk sac tumor contains tissues from all three germ layers, including ectodermal, mesodermal, and endodermal tissues.

5. Correct. Schiller-Duval bodies are a unique feature of yolk sac tumor, and it also secretes AFP.

Types of Ovarian Tumours

There are four main types of ovarian tumours, including surface derived tumours, germ cell tumours, sex cord-stromal tumours, and metastasis. Surface derived tumours are the most common, accounting for around 65% of ovarian tumours, and include the greatest number of malignant tumours. These tumours can be either benign or malignant and include serous cystadenoma, serous cystadenocarcinoma, mucinous cystadenoma, mucinous cystadenocarcinoma, and Brenner tumour. Germ cell tumours are more common in adolescent girls and account for 15-20% of tumours. These tumours are similar to cancer types seen in the testicle and can be either benign or malignant. Examples include teratoma, dysgerminoma, yolk sac tumour, and choriocarcinoma. Sex cord-stromal tumours represent around 3-5% of ovarian tumours and often produce hormones. Examples include granulosa cell tumour, Sertoli-Leydig cell tumour, and fibroma. Metastatic tumours account for around 5% of tumours and include Krukenberg tumour, which is a mucin-secreting signet-ring cell adenocarcinoma resulting from metastases from a gastrointestinal tumour.

Smoking while pregnant is associated with a higher likelihood of having a baby that is small for gestational age. The increased risk is thought to be due to exposure to nicotine and carbon monoxide. Diabetes mellitus, previous pregnancy, and maternal obesity are not linked to small for gestational age babies, but rather to large for gestational age babies.

Small for Gestational Age (SGA) is a statistical definition used to describe babies who are smaller than expected for their gestational age. Although there is no universally agreed percentile, the 10th percentile is often used, meaning that 10% of normal babies will be below this threshold. SGA can be determined either antenatally or postnatally. There are two types of SGA: symmetrical and asymmetrical. Symmetrical SGA occurs when the fetal head circumference and abdominal circumference are equally small, while asymmetrical SGA occurs when the abdominal circumference slows relative to the increase in head circumference.

There are various causes of SGA, including incorrect dating, constitutionally small (normal) babies, and abnormal fetuses. Symmetrical SGA is more common and can be caused by idiopathic factors, race, sex, placental insufficiency, pre-eclampsia, chromosomal and congenital abnormalities, toxins such as smoking and heroin, and infections such as CMV, parvovirus, rubella, syphilis, and toxoplasmosis. Asymmetrical SGA is less common and can be caused by toxins such as alcohol, cigarettes, and heroin, chromosomal and congenital abnormalities, and infections.

The management of SGA depends on the type and cause. For symmetrical SGA, most cases represent the lower limits of the normal range and require fortnightly ultrasound growth assessments to demonstrate normal growth rates. Pathological causes should be ruled out by checking maternal blood for infections and searching the fetus carefully with ultrasound for markers of chromosomal abnormality. Asymmetrical SGA also requires fortnightly ultrasound growth assessments, as well as biophysical profiles and Doppler waveforms from umbilical circulation to look for absent end-diastolic flow. If results are sub-optimal, delivery may be considered.

Placental abruption, placenta praevia, and ectopic pregnancy can cause vaginal bleeding, but they do not typically result in a non-tender, large-for-dates uterus. Gestational diabetes is not associated with vaginal bleeding or hyperemesis.

Molar pregnancy is a type of gestational trophoblastic disease that occurs when there is an abnormal fertilization of an empty ovum. There are two types of molar pregnancies: complete and partial. Complete hydatidiform moles have a karyotype of 46 XX or 46 XY, with all genetic material coming from the father. Partial hydatidiform moles have a karyotype of 69 XXX or 69 XXY and contain both maternal and paternal chromosomes. Neither type of molar pregnancy can result in a viable fetus.

The most common symptom of a molar pregnancy is vaginal bleeding, which can range from light to heavy. In about 25% of complete molar pregnancies, the uterus may be larger than expected for the gestational age. Complete hydatidiform moles produce high levels of beta hCG due to the large amounts of abnormal chorionic villi, which can lead to hyperemesis, hyperthyroidism, and other symptoms. Women who are under 20 years old or over 35 years old are at a higher risk of having a molar pregnancy.

Gestational trophoblastic disorders refer to a range of conditions that originate from the placental trophoblast. These disorders include complete hydatidiform mole, partial hydatidiform mole, and choriocarcinoma. Complete hydatidiform mole is a benign tumor of trophoblastic material that occurs when an empty egg is fertilized by a single sperm that duplicates its own DNA, resulting in all 46 chromosomes being of paternal origin. Symptoms of this disorder include bleeding in the first or early second trimester, exaggerated pregnancy symptoms, a large uterus for dates, and high levels of human chorionic gonadotropin (hCG) in the blood. Hypertension and hyperthyroidism may also be present. Urgent referral to a specialist center is necessary, and evacuation of the uterus is performed. Effective contraception is recommended to avoid pregnancy in the next 12 months. About 2-3% of cases may progress to choriocarcinoma. In partial mole, a normal haploid egg may be fertilized by two sperms or one sperm with duplication of paternal chromosomes, resulting in DNA that is both maternal and paternal in origin. Fetal parts may be visible, and the condition is usually triploid.

Gestational diabetes is the correct answer as it can result in foetal macrosomia, which is caused by insulin resistance promoting fat storage, and polyhydramnios, which is caused by foetal polyuria.

While maternal obesity may cause macrosomia, it does not necessarily lead to polyhydramnios.

Foetal gut atresia is a condition where part of the intestine is narrowed or absent, which can make it difficult for the foetus to ingest substances like amniotic fluid. This can result in excess amniotic fluid and polyhydramnios, but not macrosomia.

Hydrops fetalis may cause polyhydramnios, but it does not necessarily lead to macrosomia. However, it can cause hepatosplenomegaly.

Maternal hypercalcaemia may cause polyhydramnios, but it does not necessarily lead to macrosomia.

Gestational diabetes is a common medical disorder that affects around 4% of pregnancies. It can develop during pregnancy or be a pre-existing condition. According to NICE, 87.5% of cases are gestational diabetes, 7.5% are type 1 diabetes, and 5% are type 2 diabetes. Risk factors for gestational diabetes include a BMI of > 30 kg/m², previous gestational diabetes, a family history of diabetes, and family origin with a high prevalence of diabetes. Screening for gestational diabetes involves an oral glucose tolerance test (OGTT), which should be performed as soon as possible after booking and at 24-28 weeks if the first test is normal.

To diagnose gestational diabetes, NICE recommends using the following thresholds: fasting glucose is >= 5.6 mmol/L or 2-hour glucose is >= 7.8 mmol/L. Newly diagnosed women should be seen in a joint diabetes and antenatal clinic within a week and taught about self-monitoring of blood glucose. Advice about diet and exercise should be given, and if glucose targets are not met within 1-2 weeks of altering diet/exercise, metformin should be started. If glucose targets are still not met, insulin should be added to the treatment plan.

For women with pre-existing diabetes, weight loss is recommended for those with a BMI of > 27 kg/m^2. Oral hypoglycaemic agents, apart from metformin, should be stopped, and insulin should be commenced. Folic acid 5 mg/day should be taken from pre-conception to 12 weeks gestation, and a detailed anomaly scan at 20 weeks, including four-chamber view of the heart and outflow tracts, should be performed. Tight glycaemic control reduces complication rates, and retinopathy should be treated as it can worsen during pregnancy.

Targets for self-monitoring of pregnant women with diabetes include a fasting glucose level of 5.3 mmol/l and a 1-hour or 2-hour glucose level after meals of 7.8 mmol/l or 6.4 mmol/l, respectively. It is important to manage gestational diabetes and pre-existing diabetes during pregnancy to reduce the risk of complications for both the mother and baby.

PPH, which is the loss of 500 millilitres or more of blood within 24 hours of delivery, is primarily caused by uterine atony. This occurs when the uterus fails to contract after the placenta is delivered. However, other potential causes must be ruled out through thorough clinical examination. To remember the causes of PPH, the acronym ‘the 4 Ts’ can be used: Tone (uterine atony), Tissue (retained products of conception), Trauma (to the genital tract or perineum), and Thrombin (coagulation abnormalities). This information is based on RCOG Green-top Guideline No. 52.

Postpartum Haemorrhage: Causes, Risk Factors, and Management

Postpartum haemorrhage (PPH) is a condition characterized by excessive blood loss of more than 500 ml after a vaginal delivery. It can be primary or secondary. Primary PPH occurs within 24 hours after delivery and is caused by the 4 Ts: tone, trauma, tissue, and thrombin. The most common cause is uterine atony. Risk factors for primary PPH include previous PPH, prolonged labour, pre-eclampsia, increased maternal age, emergency Caesarean section, and placenta praevia. Management of PPH is a life-threatening emergency that requires immediate involvement of senior staff. The ABC approach is used, and bloods are taken, including group and save. Medical management includes IV oxytocin, ergometrine, carboprost, and misoprostol. Surgical options are considered if medical management fails to control the bleeding. Secondary PPH occurs between 24 hours to 6 weeks after delivery and is typically due to retained placental tissue or endometritis.

Understanding Postpartum Haemorrhage

Postpartum haemorrhage is a serious condition that can occur after vaginal delivery. It is important to understand the causes, risk factors, and management of this condition to ensure prompt and effective treatment. Primary PPH is caused by the 4 Ts, with uterine atony being the most common cause. Risk factors for primary PPH include previous PPH, prolonged labour, and emergency Caesarean section. Management of PPH is a life-threatening emergency that requires immediate involvement of senior staff. Medical management includes IV oxytocin, ergometrine, carboprost, and misoprostol. Surgical options are considered if medical management fails to control the bleeding. Secondary PPH occurs between 24 hours to 6 weeks after delivery and is typically due to retained placental tissue or endometritis. It is important to be aware of the signs and symptoms of PPH and seek medical attention immediately if they occur.

The external oblique aponeurosis provides the outermost layer of the spermatic cord, which is acquired during its passage through the superficial inguinal ring.

Anatomy of the Scrotum and Testes

The scrotum is composed of skin and dartos fascia, with an arterial supply from the anterior and posterior scrotal arteries. It is also the site of lymphatic drainage to the inguinal lymph nodes. The testes are surrounded by the tunica vaginalis, a closed peritoneal sac, with the parietal layer adjacent to the internal spermatic fascia. The testicular arteries arise from the aorta, just below the renal arteries, and the pampiniform plexus drains into the testicular veins. The left testicular vein drains into the left renal vein, while the right testicular vein drains into the inferior vena cava. Lymphatic drainage occurs to the para-aortic nodes.

The spermatic cord is formed by the vas deferens and is covered by the internal spermatic fascia, cremasteric fascia, and external spermatic fascia. The cord contains the vas deferens, testicular artery, artery of vas deferens, cremasteric artery, pampiniform plexus, sympathetic nerve fibers, genital branch of the genitofemoral nerve, and lymphatic vessels. The vas deferens transmits sperm and accessory gland secretions, while the testicular artery supplies the testis and epididymis. The cremasteric artery arises from the inferior epigastric artery, and the pampiniform plexus is a venous plexus that drains into the right or left testicular vein. The sympathetic nerve fibers lie on the arteries, while the parasympathetic fibers lie on the vas. The genital branch of the genitofemoral nerve supplies the cremaster. Lymphatic vessels drain to lumbar and para-aortic nodes.

The drainage of the testicles starts in the septa, where the veins of the tunica vasculosa and the pampiniform plexus come together at the back of the testis. From there, the pampiniform plexus leads to the testicular vein, which then drains into either the left renal vein or the inferior vena cava, depending on which testicle it comes from.

Anatomy of the Scrotum and Testes

The scrotum is composed of skin and dartos fascia, with an arterial supply from the anterior and posterior scrotal arteries. It is also the site of lymphatic drainage to the inguinal lymph nodes. The testes are surrounded by the tunica vaginalis, a closed peritoneal sac, with the parietal layer adjacent to the internal spermatic fascia. The testicular arteries arise from the aorta, just below the renal arteries, and the pampiniform plexus drains into the testicular veins. The left testicular vein drains into the left renal vein, while the right testicular vein drains into the inferior vena cava. Lymphatic drainage occurs to the para-aortic nodes.

The spermatic cord is formed by the vas deferens and is covered by the internal spermatic fascia, cremasteric fascia, and external spermatic fascia. The cord contains the vas deferens, testicular artery, artery of vas deferens, cremasteric artery, pampiniform plexus, sympathetic nerve fibers, genital branch of the genitofemoral nerve, and lymphatic vessels. The vas deferens transmits sperm and accessory gland secretions, while the testicular artery supplies the testis and epididymis. The cremasteric artery arises from the inferior epigastric artery, and the pampiniform plexus is a venous plexus that drains into the right or left testicular vein. The sympathetic nerve fibers lie on the arteries, while the parasympathetic fibers lie on the vas. The genital branch of the genitofemoral nerve supplies the cremaster. Lymphatic vessels drain to lumbar and para-aortic nodes.