Up to 20% of women have been found to have Group B streptococcus (GBS). GBS is considered a normal flora of the gastrointestinal tract. GBS infection is generally asymptomatic although some women might end up having a UTI. Infants born to mothers who are colonised with GBS during labour are at a higher risk of developing early-onset GBS infection. If a pregnant woman develops a UTI due to GBS, it is suggestive of significant GBS colonisation. IV penicillin would be the drug of choice and is to be administered to the mother during labour which would provide sufficient protection for the foetus and would be effective enough. If penicillin is unavailable, ampicillin is a reasonable alternative. If a patient has penicillin allergy, vancomycin can be used. If not for penicillin, roughly 50% of babies delivered vaginally to women who are GBS positive would be colonised with the organism and out of this percentage, 1-2% can go on to develop a severe infection such as septicaemia and meningitis which could often be fatal.

IM penicillin can be administered to the newborn immediately post-delivery would be an effective prophylaxis in most cases but one should not wait until signs of infection are present to give the injection. Many newborns would still have an immature immune system which could cause some to die. Hence, it is more suitable to treat all women who tested positive during labour and the newborn as well if any signs of infection do appear. The majority of babies don’t need antibiotic treatment if their mother has been treated.

Lymphatic drainage of the bladder is to the common iliac nodes via the internal iliac nodes.

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.

There are no interactions between the combined oral contraceptive pill, progesterone-only pill, medroxyprogesterone injections or levonorgestrel implants and the AEDs valproic acid (sodium valproate), vigabatrin, lamotrigine, gabapentin, tiagabine, levetiracetam, zonisamide, ethosuximide and the benzodiazepines. So she can use COCP along with Sodium valproate.

The round ligament develops from the lower end of the gubernaculum in females. In the males it persists as the scrotal ligament.

Ovulation usually occurs on day 14 in a typical 28-day cycle. Luteinizing hormone levels spike as a result of increased oestrogen levels secreted from maturing follicles. This LH spike occurs about 24-36 hours before the release of the oocyte from the mature follicle.

The first sign of puberty in females is the development of breasts.

The following treatment regimes are recommended for the treatment of Chlamydia in Pregnancy: Erythromycin 500mg four times a day for 7 days or Erythromycin 500 mg twice a day for 14 days or Amoxicillin 500 mg three times a day for 7 days or Azithromycin 1 gm stat (only if no alternative, safety in pregnancy not fully assessed) The following treatment regimes are recommended for the treatment of Chlamydia in NON-PREGNANT patients: Doxycycline 100mg bd for 7 days OR Azithromycin 1gm orally in a single dose NOTE: Doxycycline and Ofloxacin are contraindicated in pregnancy

Fat necrosis is a benign (non-cancerous) breast condition that can develop when an area of fatty breast tissue is injured. It can also develop after breast surgery or radiation treatment.

There are different stages of fat necrosis. As the fat cells die, they release their contents, forming a sac-like collection of greasy fluid called an oil cyst. Over time, calcifications (small deposits of calcium) can form around the walls of the cyst, which can often be seen on mammograms. As the body continues to repair the damaged breast tissue, it’s usually replaced by denser scar tissue. Oil cysts and areas of fat necrosis can form a lump that can be felt, but it usually doesn’t hurt. The skin around the lump might look thicker, red, or bruised. Sometimes these changes can be hard to tell apart from cancers on a breast exam or even a mammogram. If this is the case, a breast biopsy (removing all or part of the lump to look at the tissue under the microscope) might be needed to find out if the lump contains cancer cells. These breast changes do not affect your risk for breast cancer.

Mastectomy, axillary node dissection and radiation therapy are all management options for malignancy which this patient doesn’t have.

Postpartum haemorrhage (PPH) is a cumulative blood loss greater than 1000 mL with signs and symptoms of hypovolemia within 24 hours of the birth process, regardless of the route of delivery.

The first step in managing hemorrhagic shock is recognition. This should occur before the development of hypotension. Close attention should be paid to physiological responses to low blood volume. Tachycardia, tachypnoea, and narrowing pulse pressure may be the initial signs.

Tachycardia is typically the first abnormal vital sign of hemorrhagic shock. As the body attempts to preserve oxygen delivery to the brain and heart, blood is shunted away from extremities and nonvital organs. This causes cold and modelled extremities with delayed capillary refill. This shunting ultimately leads to worsening acidosis.