Revise Notes Obg Flashcards

1
Q

Amenorrhoea
Background

Amenorrhoea is the absence of menstruation. It is classified into primary & secondary:

Primary amenorrhoea - the failure to commence menstruation by the age of expected menarche

Usually 15 yrs if otherwise normal sexual development or..

13 years if no secondary sexual characteristics

Secondary amenorrhoea - the cessation of menstruation in a women with previous menses for 3 months (or 6 months if Hx oligomenorrhoea)

A

Causes of Amenorrhoea

Primary amenorrhoea

If normal secondary sexual characteristics, amenorrhoea can be caused by:

❤️Constitutional delay - usually a family history
Endocrine - Thyroid dysfunction, hyperprolactinaemia, Cushing’s

❤️Androgen insensitivity syndrome
If the patient has no secondary sexual characteristics (e.g. breast development), amenorrhoea can reflect:

❤️Primary ovarian insufficiency - commonly Turner’s syndrome (46XO)
Suggested by short stature, shield chest, wide carrying angle, scoliosis, web neck

❤️Hypothalamic dysfunction - e.g. stress/ excess weight loss/exercise (e.g. in endurance athletes/eating disorders)

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2
Q

Secondary amenorrhea

A

Secondary amenorrhoea

If there is hyperandrogenism (e.g. hirsutism/acne), causes include:

❤️PCOS
❤️Cushing’s syndrome

If there is no evidence of hyperandrogenism:

❤️Physiological - pregnancy/lactation, menopause

❤️Premature ovarian insufficiency
FSH > 20 in a F < 40 yrs is suggestive of ovarian failure

❤️Hypothalamic dysfunction as above

❤️Pituitary causes - Prolactinoma

❤️Thyroid dysfunction

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3
Q

Investigating Amenorrhoea

Assessment of Primary Amenorrhoea

Referral to a specialist is recommended. Investigations may include:

A

❤️Pelvis US - to r/o absent uterus / abnormal development of genital organs

❤️Serum prolactin - if > 1000 invx for prolactinoma

❤️TFTs

❤️FSH and LH - if elevated, can suggest primary ovarian failure - Turner’s syndrome

❤️Total testosterone - if evidence of hyperandrogenism (acne, hirsutism etc.)
—If elevated can suggest androgen insensitivity syndrome
—If moderately increased, can support a diagnosis of PCOS

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4
Q

Assessment of Secondary Amenorrhoea

Investigations may include

A

❤️FSH/LH
—-Elevated FSH/LH are suggestive of premature ovarian insufficiency in women < 40 yrs

—-If FSH is normal, and LH is moderately increased - can suggest PCOS

—-If FHS/LH are low/normal - can suggest a hypothalamic cause (e.g. weight loss)

❤️Prolactin levels
❤️TFTs
❤️Testosterone

❤️US - to investigate for polycystic ovaries (12 or more follicles / volume > 10cm3)

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5
Q

Turner Syndrome

Pathophysiology

Genetics 45 X,O
1/2500 females
Clinical features

Short stature – growth rate falters after 3-5yrs (skeletal dysplasia)
Broad ‘webbed’ neck;

Wide carrying angle at elbows (cubitus valgus)
Shield chest with widely-spaced hypoplastic nipples

Primary amenorrhoea
Hypothyroidism - approximately 1/3rd of patients develop Hashimoto’s thyroiditis

A

Associated abnormalities

CHD – coarctation of the aorta ; VSD
Renal – horseshoe kidney / unilateral agenesis
Hypoplastic ‘streak’ ovaries – primary amenorrhoea and infertility

Diagnosis & Management

Diagnosis: Karyotyping
Management
S/C HGH +/- anabolic steroids
Oral oestrogen – induce puberty

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6
Q

Polycystic Ovarian Syndrome [PCOS]

A very common disorder affecting an estimated 5-15% of the population.

Pathology: Multifactorial, involving insulin resistance, hyperinsulinemia and hormonal imbalance (elevated LH & androgens)

Clinical features

Oligo/amenorrhoea
Impaired fertility - so often present with difficulty conceiving
Evidence of hyperandrogenism - hirsutism, acne
Evidence of insulin resistance:
Acanthosis nigricans
Obesity

A

Investigations

Bloods:
Increased LH:FSH ratio
Moderately elevated testosterone levels
Sex hormone binding globulin levels are low
Pelvis USS - ovarian cysts
Diagnosis

The Rotterdam criteria - a diagnosis of PCOS can be made if 2/3 criteria are present:

Olgio/amenorrhoea
Hyperandrogenism - acne, hirsutism, biochemical evidence
Cysts - 12 or more follicles in at least one ovary OR > 10cm3 total ovarian volume

Management

Hirsutism + acne
1st line - COCP
Infertility
Weight loss
Clomifene - most effective measure, can be complicated by multiple pregnancies
Metformin

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7
Q

The Menstrual Cycle (Follicular vs Luteal)

The menstrual cycle can be divided into 4 core phases. The duration of each phase varies between individuals

A

Phase 1: Menstruation

Menstruation occurs between DAY 1- 4
Phase 2: The Proliferative (Follicular) Phase – DAY 5-13

Ovarian changes
During the proliferative phase, the ovarian follicles develop.
One follicle becomes the ‘dominant’ follicle.

Endometrial changes
The endometrial tissue proliferates

Hormonal changes
Follicle stimulating hormone (FSH) increases – this stimulates follicle development

The developing follicles secrete increasing amounts of oestradiol
When the dominant follicle has matured, there is a significant increase in OESTRADIOL which TRIGGERS AN ACUTE INCREASE IN LUTEINIZING HORMONE (LH).
The acute rise in LH TRIGGERS OVULATION (LH surge)

Cervical mucus:
Initially thick, but prior to ovulation becomes clear, thin and ‘stretchy’
Basal body temperatures decreases just before ovulation occurs.

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8
Q

The Menstrual Cycle (Follicular vs Luteal)

The menstrual cycle can be divided into 4 core phases. The duration of each phase varies between individuals

A

Phase 3: Ovulation – DAY 14

Phase 4: The Secretory (luteal) Phase – Day 15-28

Ovarian changes:
An ovarian follicle forms into the CORPUS LUTEUM after the release of the oocyte during ovulation
The corpus luteum SECRETES PROGESTERONE

Endometrial changes
Progesterone stimulates changes to the endometrium to form a ‘secretory’ lining.

Hormonal changes:
If fertilisation does NOT occur, the corpus luteum degenerates, resulting in a FALL IN PROGESTERONE (as well as an increase in oestradiol) – this leads to menstruation

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9
Q

Uterine prolapse mng

A

Management

❤️Pelvic Floor Muscle Training

💕Kegel Exercises: Pelvic floor exercises to strengthen the levator ani and associated muscles.

💕Physiotherapy: Pelvic floor rehabilitation guided by a specialist physiotherapist.

❤️Pessary Device

💕Ring Pessary: A non-surgical device inserted into the vagina to provide structural support to the prolapsed uterus.

❤️Surgical Management

💕Colporrhaphy: Vaginal wall repair to reinforce the vaginal fascia and improve support.

💕Uterine suspension procedures: Sacrospinous fixation, uterosacral ligament suspension, or sacrohysteropexy using native tissue or synthetic mesh.

💕Hysterectomy: Vaginal or abdominal removal of the uterus, often combined with pelvic floor repair procedures.

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10
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11
Q

Uterine Prolapse
Descent of the pelvic organs into the vagina as a result of weakness of the muscles of the pelvic floor and supporting ligaments

❤️Pathophysiology

Pelvic organ prolapse (POP) occurs when the pelvic floor muscles, ligaments, and connective tissue lose their integrity.

❤️Contributing factors include

vaginal deliveries,

ageing (post-menopausal) and

chronic intra-abdominal pressure (obesity, chronic cough, or heavy lifting).

A

Clinical Features

❤️A chronic dragging sensation or pelvic heaviness.

Patients often report a sensation of a vaginal mass or “something coming down,” which may be visible on physical examination.

❤️Urinary Symptoms - stress incontinence, urgency, frequency, and incomplete voiding due to bladder outlet obstruction.

❤️Bowel Symptoms - Constipation, straining, incomplete evacuation.

❤️Sexual Dysfunction - dyspareunia, reduced sexual sensation, and difficulty with coitus

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12
Q

Antenatal Care
Gestational Diabetes

The second most common complication of pregnancy (after hypertension), affecting approximately 1 in 40 pregnancies.

Risk factors

💕Ethnicity (Asian, African-Carribean)
💕Obesity - BMI > 30

💕Previous macrosomia (newborn >4.5kg)
💕Previous gestational diabetes
💕1st relative with diabetes

A

Investigations

💕Screening

💕Patients without risk factors should be screened with the Oral Glucose Tolerance Test (OGTT)

at 24-28 weeks

💕Patients who have any of the above risk

factors should be screened for GDM with an OGTT at booking AND at 24-28 weeks.

💕Diagnosis

Fasting BM > 5.6
OGTT > 7.8
Tip: GDM - 5, 6, 7, 8

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13
Q

BM targets for GDM/DM during pregnancy

A

Fasting target - 5.3
1 hour post-meal target 7.8
2 hour post-meal target 6.4

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14
Q

Gestational Diabetes

The second most common complication of pregnancy (after hypertension), affecting approximately 1 in 40 pregnancies.

Mng

A

Management

Management if fasting BM < 7

❤️If fasting BM is < 7 - trial diet and exercise for 2 weeks
💕If BM is still too high (see targets below), add metformin
💕If BM remains too high despite metformin, treat with insulin, metformin and diet/exercise

❤️Management if fasting BM > 7 (or FBM 6.1-6.9 and complicated pregnancy (macrosomia, hydramnios etc.))

Commence insulin as first step

❤️Management of Pre-existing diabetes in pregnancy

💕Diabetic control:
All oral hypoglycaemics should be stopped
Continue metformin
Start insulin

Additional measures

💕Prescribe high dose folic acid 5mg OD until 12 weeks (high risk of neural tube defects)

💕Aspirin 75mg OD from 12 weeks (high risk of pre-eclampsia)

💕Detailed anomaly scan at 20 weeks + 4 chamber echo.

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15
Q

Antenatal Care

Imaging

Dating scan - Ultrasound at 11-14 weeks
Fetal anomaly scan - 18-21 weeks

A

Combined test

💕10-13 weeks - nuchal lucency and blood tests for PAPP &
b-hcg levels - the value of these 3 markers gives the

💕estimated risk of Down syndrome (trisomy 21), Edwards Syndrome (trisomy 18), Patau syndrome (trisomy 13)

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16
Q

Further investigations

If combined test result is > 1:150 risk = ‘higher chance’ - offer women the following:

A

Further investigations

❤️If combined test result is > 1:150 risk = ‘higher chance’ - offer women the following:

❤️Non-invasive prenatal testing (blood test)

Measures DNA released from placenta into maternal bloodstream. Quantifies DNA from chromosome 21, 18, 13

Results: Low chance or High chance - then offer diagnostic testing

❤️Chorionic villus sampling at < 13 weeks

❤️Amniocentesis at > 15 weeks
The additional risk of misscarriage following CVS or amniocentesis is likely to be < 0.5%

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17
Q

Booking and 28 week appointment

A

❤️Booking appointment

💕Screen for GDM if RFs (as above)
Screen for pre-eclampsia (if high risk - aspirin from 12 weeks)

💕Check blood pressure and urine dip (for proteinuria)
Recheck at each appointment thereafter

💕Check FBC, blood group and Rh status

❤️28 week appointment

💕Offer anti-D prophylaxis to rhesus-negative women
💕Repeat at 31-34 weeks if following 2 dose regimen

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18
Q

Supplements

A

Supplements

💕Folic acid - to reduce risk of neural tube defects - take for at least first 12 weeks of pregnancy

💕Most women should take 400 micrograms OD

💕For women at high risk of NTDs (previous child with NTD,
AEDs, diabetes,
coeliac,
sickle/thalassaemia,
BMI > 30) -
take 5 milligrams per day

💕Advise all women to take 10mcg Vit D OD throughout pregnancy

💕Avoid vitamin A supplementation - birth defects

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19
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20
Q

Secondary amenorrhea

A

Secondary amenorrhoea

If there is hyperandrogenism (e.g. hirsutism/acne), causes include:

❤️PCOS
❤️Cushing’s syndrome

If there is no evidence of hyperandrogenism:

❤️Physiological - pregnancy/lactation, menopause

❤️Premature ovarian insufficiency
FSH > 20 in a F < 40 yrs is suggestive of ovarian failure

❤️Hypothalamic dysfunction as above

❤️Pituitary causes - Prolactinoma

❤️Thyroid dysfunction

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21
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23
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24
Q

Screening test

A

UK National Cancer Screening Programmes
Key learning

UK National Cancer Screening Programmes:

💕Cervical Cancer:
Women aged 24.5-64.
Ages 25-49: Every 3 years; Ages 50-64: Every 5 years.
Screening via cervical smear and HPV test.
Abnormal results lead to cytology, colposcopy, and treatment or rescreening.

💕Breast Cancer:
Women aged 47-73, every 3 years.
Mammography for most, MRI for high-risk young women.
Triple assessment for abnormal results. DCIS treated as cancer.

💕Bowel Cancer:

Ages 60-74, every 2 years.
Faecal occult blood test (FOBT); abnormal results lead to colonoscopy.

💕Abdominal Aortic Aneurysm
Men aged 65 - ultrasound to measure abdominal aortic diameter

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1) Cervical cancer screening Offered to all women aged 24.5-64 25-49 screened every 3 years 50-64 every 5 years Screened through cervical smear Smear sent for HPV test
If positive -> cytological examination and cytology-> if abnormal-> colposcopy Treat if cancer or rescreen at 1/3/5 years / repeat colposcopy depending on results Poorest uptake in highest risk patients (low socio-economic background and high sexual activity)
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2) Breast cancer screening Offered to all women aged 47-73 Every 3 years If over 70 can ask for screening through GP Screening involves mammography
Screening involves mammography MRI can be used for young women at high risk due to family history Separate high risk surveillance screening for those with known BRCA/TP53 mutations or strong family history Breast cancer incidence has increased since screening due to high levels of detection of ductal carcinoma in-situ (DCIS)- treated as cancer but may not ever invade surrounding tissue Screening Outcomes If a breast cancer screening test is abnormal, the patient will undergo triple assessment of the breast If triple assessment is normal, the patient will return to the normal screening programme If cancer is detected (including DCIS) it will be treated There is a 10% false negative rate
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3) Bowel cancer screening Offered to all aged 60-74 Every two years If above 74 can request screening via GP Screening via faecal occult blood test (FOBT) If abnormal-> colonoscopy If unclear-> repeat FOBT If normal-> continue screening every 2 years Colonoscopy:
Colonoscopy: Clear- return to screening Cancer- treat Polyp- removed and analysed and risk stratified: Low risk- continue FOBT screening Medium risk- Colonoscopy every 3 years High risk- Colonoscopy in 12 months then 3 yearly 0.1% samples= cancer- majority confined to bowel 0.5%= polyps
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Similarly to breast cancer there are also moderate/high risk surveillance groups- via regular OGD/colonoscopy
High risk groups: First degree relative bowel cancer < 50 Familial adenomatous polyposis (FAP) Hereditary non-polyposis colorectal cancer (HNPCC) Inflammatory bowel disease (IBD) Acromegaly
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4. Abdominal Aortic Aneurysm screening In the UK, the Abdominal Aortic Aneurysm (AAA) Screening Program targets men aged 65 and older. Screening is done using an ultrasound to measure the aortic diameter
. Diagnosis Threshold: An aortic diameter ≥3 cm confirms an AAA. Monitoring: Small AAA (3.0–4.4 cm): Annual ultrasound surveillance. Medium AAA (4.5–5.4 cm): Surveillance every 3 months. Large AAA (≥5.5 cm): Consideration for elective surgery due to increased rupture risk. Elective Surgical Management: Surgery is recommended for large AAAs (≥5.5 cm) or if the aneurysm grows ≥1 cm per year. Options include open surgical repair or endovascular aneurysm repair (EVAR), with choice depending on patient suitability and risk assessment.
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Other examples of regular screening: Liver: HCC: 6 monthly abdominal USS and AFP for all chronic liver disease patients Variceal screening: Every 1-3 years for those with confirmed varices Liver cirrhosis: Annual Fibroscan screening if Hep C, alcoholic liver disease, heavy drinkers Cholangiocarcinoma: Annual USS and CA19-9 in all patients with primary sclerosing cholangitis Renal
Renal: Adult polycystic kidney disease: Regular US kidneys for relatives of patients Diabetes (known diabetics): Diabetic foot disease: annual screening Diabetic retinopathy: annual screening Genetic screening examples: Cystic fibrosis: CFTR gene mutation Haemochromatosis: HFE gene mutations
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Summary of screening program
Screening Programmes Cancer Screening Programme Target Population Screening Test Frequency Purpose Breast Cancer Screening Women aged 43-73 Mammography Every 3 years Early detection of breast cancer including DCIS Cervical Cancer Screening Women aged 25-64 Cervical smear Every 3-5 years Detection of abnormal cervical cells Bowel Cancer Screening Men and women aged 60-74 Faecal occult blood test (FOBT) Every 2 years Detection of blood in stool Summary of UK National Cancer Screening Programme Sensitivity and Specificity Cancer Screening Programme Sensitivity Specificity Breast Cancer Screening Approx. 80% Approx. 90% Cervical Cancer Screening Approx. 80-90% Approx. 90-95% Bowel Cancer Screening Approx. 60-70% Approx. 90%
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Transient tachypnoea of the newborn A benign, self-limiting condition. The commonest cause of respiratory distress in newborns Pathophysiology TTN is caused by delayed clearance of foetal lung fluid, leading to impaired gas exchange and respiratory distress. Clinical Features TTN typically presents within the first few hours of life. Tachypnoea (>60 breaths/min) Respiratory distress - nasal flaring, grunting, subcostal/intercostal recessions. Symptoms usually resolve within 24-72 hours.
Risk Factors Risk factors for TTN include: Caesarean section Prematurity (especially late preterm, 34-37 weeks) Rapid labor and delivery Investigations Chest X-ray - hyperinflation, fluid in the fissures, and occasional pleural effusions. Management TTN is usually self-limiting. Management focuses on supportive care: Oxygen therapy to maintain adequate oxygen saturation Nasal CPAP (Continuous Positive Airway Pressure) in severe cases TTN typically resolves within 72 hours, with most infants recovering fully without long-term complications.
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Shoulder dystocia Shoulder dystocia is an obstetric emergency where either the anterior or less commonly the posterior, foetal shoulder impacts on and 'gets stuck' behind the maternal symphysis, or sacral promontory, respectively. This requires additional manoeuvers after head delivery. It can cause significant perinatal morbidity, including brachial plexus injury, postpartum hemorrhage, and severe perineal tears, despite appropriate management. Figure 207: Shoulder dystocia - Note the anterior shoulder impacting on the maternal pubic symphysis. Henry Lerner. Suprapubic-pressureforSD, CC BY 4.0
Risk Factors Maternal diabetes Foetal macrosomia Maternal obesity Prolonged second stage of labor History of shoulder dystocia Instrumental delivery (use of forceps or vacuum) Clinical features Difficulty in delivering the foetal shoulders after the head has been delivered . "Turtle sign": the foetal head retracts against the perineum after it has emerged. Management Manoeuvres including McRoberts Manoeuvre Hyperflex the mother’s legs tightly to her abdomen to flatten the sacrum and rotate the symphysis pubis. RCOG: “McRobert’s is a simple, rapid and effective intervention and should be performed first” Other manoeuvres include : Rubin’s Manoeuver: Apply pressure on the accessible shoulder to push it towards the chest. Wood's Screw Maneuver: Rotate the posterior shoulder to release the impacted anterior shoulder. Delivery of Posterior Arm: Insert a hand into the vagina, locate the posterior arm, and gently pull it out. Gaskin Manoeuver: Position the mother on all fours to widen the pelvis. Suprapubic pressure should be applied Episiotomy can be required Prevention: Optimal management of gestational diabetes Consider elective cesarean delivery in cases of suspected foetal macrosomia or prior shoulder dystocia
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Complication of shoulder dystocia
Complications For the baby: Brachial plexus injury Fractures (clavicle, humerus) Hypoxia, or death. For the mother: Postpartum haemorrhage Perineal tears Uterine rupture.
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Sheehan Syndrome Pathophysiology Sheehan syndrome describes excessive blood loss during labour or postpartum haemorrhage (PPH), leading to ischaemic necrosis of the pituitary gland. This results in hypopituitarism Clinical Features Presentations include lactation failure, amenorrhea, fatigue, and various hormonal deficiencies such as hypothyroidism and adrenal insufficiency. Severe cases may manifest as panhypopituitarism.
Diagnosis Diagnosis involves clinical suspicion based on history of significant postpartum haemorrhage and symptoms. Hormonal assays confirm pituitary hormone deficiencies. Management Hormone replacement therapy (e.g., corticosteroids, levothyroxine, oestrogen/progesterone replacement) tailored to specific deficiencies. Regular monitoring and adjustment of replacement therapy optimise patient outcomes.
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Round Ligament Pain Round ligament pain is a common cause of abdominal discomfort during pregnancy, typically occurring in the second trimester. Diagnosis is clinical, and suggested by sharp/stabbing groin pain triggered by movement, in the 2nd trimester. Pathophysiology The round ligaments extend from the uterine horns to the labia majora via the inguinal canal. During pregnancy, these ligaments stretch and thicken to accommodate the growing uterus, leading to pain. Sudden movements, such as standing up quickly, coughing, or rolling over in bed, can cause the ligaments to spasm/contract abruptly, resulting in sharp pain.
Clinical Features Commonly presents in 2nd trimester - most common in weeks 12-22. Sharp, stabbing pain, exacerbated by movements such as standing up/coughing etc. Most commonly felt in groin/lower abdomen (more common in right groin) or bilaterally. Management Conservative - rest, avoidance of sudden movements, simple analgesia, maternity support belts, stretching.
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Differential diagnosis - Pubic Symphysis Dysfunction
Often triggered by pregnancy due to increased laxity of ligaments Clinical features: Pain over the pubic symphysis which radiates into the groins, a ‘waddling’ gait
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Preterm Prelabour Rupture of Membranes (PPROM) Preterm prelabour rupture of membranes (PPROM) occurs when the foetal membranes rupture before 37 weeks of gestation and prior to the onset of labour, leading to significant maternal and neonatal complications. Clinical Features Sudden gush or continuous leakage of fluid from the vagina. Patients may report increased vaginal discharge May be signs of infection.
Management Treatment depends on gestational age, infection status, and foetal condition: Antibiotic Therapy: Administered to prolong pregnancy and prevent infection. Prophylactic erythromycin 250mg QDS to prevent infective chorioamnionitis Corticosteroids: To enhance foetal lung maturity if the gestational age is 24-34 weeks. Two x 12-mg doses of IM betamethasone 24 hours apart or.. Four x 6-mg doses of IM dexamethasone every 12 hours Expectant management vs Delivery: Expectant Management: In the absence of infection and with stable conditions, close monitoring in a hospital setting. Delivery: Indicated if there are signs of infection, foetal distress, or if the pregnancy reaches 34-37 weeks depending on the clinical scenario. Complications Chorioamnionitis Neonatal sepsis Umbilical cord prolapse Preterm birth with associated neonatal morbidity and mortality.
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Postpartum Haemorrhage Summary Significant bleeding after delivery of the baby and placenta. > 500ml following vaginal delivery >1L following c-section Primary PPH Haemorrhage occurring within 24 hours of delivery Causes - The four Ts Tone - uterine atony - most common Thrombin - disordered coagulation Trauma - e.g. perineal tear Tissue - retained placenta
Management The usual A-E management, resuscitation with packed red cells, FFP etc. Mechanical management - ‘massaging’ the uterus (to stimulate contraction and increase tone) Medical management: IV oxytocin - strengthens/improves uterine contractions/tone IV ergometrine - stimulates uterine and vascular smooth muscle contraction CI: HTN IM carboprost - PG analogue - stimulates contraction of uterus, improving tone Caution: Asthma Sublingual misoprostol - PG analogue Tranexamic acid Surgical - IU balloon tamponade, hysterectomy
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Placenta accreta
Placenta Accreta Can be a cause of significant PPH Pathology: Implantation of the placenta beyond the endometrium, and into the myometrium resulting in great difficulty separating the placenta during delivery --> PPH RFs: history of c-section, increasing maternal age Diagnosis: TVUS during antenatal care Management: Planned c-section with antenatal steroids, with subsequent uterus preserving surgery or hysterectomy (safest)
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Secondary PPH Bleeding which occurs from 24 hrs to 12 weeks after delivery Causes Infection - endometritis Foul-smelling discharge, bleeding, abdominal pain, pyrexia Retained products
Investigations US to r/o retained products, swabs Management Antibiotics for endometritis or surgical removal of retained products
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Pelvic Inflammatory Disease Pathophysiology Infection of the upper genital tract, which occurs when infection ascends from the endocervix, resulting in endometritis, salpingitis, oophritis etc. Aetiology: Chlamydia and Gonorrhoea account for roughly 1/4 of cases Others: Mycoplasma genitalium RFs: 4-6 weeks post IUD insertion, age < 25, recent TOP Clinical Features Symptoms Lower abdominal pain Deep dyspareunia Vaginal discharge (often purulent) Vaginal bleeding - IMB, PCB
Examination findings Bimanual exam - adnexal tenderness, cervical excitation/motion tenderness SIRS, pyrexia Investigations Clinical assessment Pregnancy test Test for causative organisms - CT/NG/MG (Nb. negative tests do not exclude PID) Bloods - elevated inflammatory markers The absence of endocervical/vaginal pus cells has a negative predictive value of 95% (but poor PPV), so is useful to r/o PID
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Mng of PID
Management BASHH recommend a low threshold for empiric treatment due to (i) lack of definitive diagnostic criteria and (ii) risk of long-term sequelae with delayed treatment (ectopic/infertility). Outpatient antibiotic regimens IM ceftriaxone 1g stat + PO doxycycline 100mg BD + PO metronidazole 400mg BD for 14 days PO ofloxacin + metronidazole for 14 days PO moxifloxacin for 14 days Inpatient antibiotic regimens IV ceftriaxone + IV doxycycline (followed by PO metronidazole + doxycycline) IV clindamycin + IV gentamicin (followed by PO clindamycin + metronidazole)
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Ovarian Torsion A gynaecological emergency resulting from torsion of the ovary, with consequent ovarian ischaemia, characterised by sudden onset severe pain in the LIF/RIF . TVUS is the primary imaging modality, demonstrating the whirlpool sign. Management is via emergency laparoscopy to de-tort the ovary. Pathophysiology Ovarian torsion involves the rotation of the ovary and part of the fallopian tube, causing the vascular pedicle to twist. This twisting can obstruct venous outflow initially, leading to ovarian oedema and subsequent arterial compromise. The resulting ischaemia, if not reversed, can cause ovarian necrosis and loss of function.
Clinical features Sudden onset pelvic pain Unilateral, affecting the LIF/RIF. Sudden onset, severe pain which worsens progressively as ischaemic time increases May be intermittent pain if the ovary intermittently untwists and retwists Nausea and vomiting Examination findings: There may be a palpable adnexal mass in the affected iliac fossa. Abdominal tenderness with guarding in the LIF/RIF. Investigations Urgent transvaginal ultrasound (TVUS) is the primary imaging modality. The "whirlpool sign" indicates the twisting of the vascular ovarian pedicle, which is highly suggestive of torsion.
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Ovarian Torsion A gynaecological emergency resulting from torsion of the ovary, with consequent ovarian ischaemia, characterised by sudden onset severe pain in the LIF/RIF. TVUS is the primary imaging modality, demonstrating the whirlpool sign. Management is via emergency laparoscopy to de-tort the ovary.
Management Surgical intervention Emergency surgery is required to detorse the ovary and restore blood flow. Laparoscopy is typically the preferred approach Oophorectomy may be necessary if the ovary is non-viable due to necrosis or if there is an associated mass or tumour Prompt recognition and surgical management of ovarian torsion are crucial to preserve ovarian function and prevent complications such as necrosis and subsequent infertility.
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Ovarian Cancer Pathophysiology 90% of ovarian tumour are epithelial carcinomas (80% serous carcinomas) Risk factors - early menarche & late menopause, BRCA 1 or 2 Clinical features Normally affects women > 50 yrs of age Frequent/persistent symptoms including: Abdominal distension/bloating Early satiety or anorexia Pelvic pain/ abdominal pain Pressure symptoms - urinary urgency or frequency Beware of diagnosing new IBS/overactive bladder in a woman > 50 years Examination: Ascites or abdominal/pelvic mass
Assessment/Investigations If ascites/mass present - refer via a 2 week wait (suspected cancer pathway) If examination is NAD - carry out assessment in primary care - 1st step: measure CA125 level If CA125 is high (>35) - arrange urgent US abdomen/pelvis If US suggests ovarian cancer, refer urgently to gynaecology for further investigation. Management: Surgery is mainstay References and Further Reading
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Obesity and Pregnancy Key learning Definition: BMI > 30 at first antenatal visit. Management: Ante-natal: Screen for gestational diabetes, folic acid 5mg (if BMI > 30), consider aspirin 150mg if BMI > 35. Intra-partum: VTE prophylaxis, early anaesthetic review. Post-partum: Weight management, breastfeeding support, plan for future pregnancies with multidisciplinary team. Definition BMI > 30 at first antenatal visit Epidemiology 21% of antenatal population are obese Only 47% of pregnant woman have a normal BMI
Complications of obesity in pregnancy : To mother: Pre-eclampsia Gestational diabetes VTE/PE Postpartum haemorrhage Requirement for induction of labour / C-section Mental health issues- anxiety/depression To fetus: Congenital anomalies Fetal macrosomia Stillbirth/neonatal death More difficult to initiate and maintain breastfeeding
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Obesity and pregnancy
Management 💕Ante-natal: Encourage to optimise weight before pregnancy Screen for gestational diabetes If BMI > 30: 5mg folic acid at least 1 month before conception and continue during first trimester If BMI > 35: Consider aspirin 150mg OD from 12 weeks gestation until birth to reduce risk of pre-eclampsia No weight loss drugs are recommended during pregnancy 💕Intra-partum management: VTE prophylaxis Early anesthetic review 💕Post-partum: Weight management Breastfeeding support MDT planning for future pregnancies
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Incomplete/missed miscarriage Expectant Management
❤️Expectant management (as above) is 1st line for incomplete/missed miscarriage, UNLESS any of the following risk factors are present (in which case, medical/surgical mx should be considered): 💕High risk of haemorrhage - e.g. late first trimester, coagulopathy 💕Previous adverse outcome - miscarriage, stillbirth, antepartum haemorrhage 💕Evidence of infection If bleeding and pain settle, this suggests a completed miscarriage, and the woman should repeat the urine pregnancy test up to 3 weeks. ❤️Medical Management Indication: Symptoms > 14 days OR not appropriate for expectant management (RFs above) 1st line - vaginal/PO misoprostol (stimulates uterine expulsion) ❤️Surgical Management Indication: Ongoing symptoms, or retained products of conception despite PO/vaginal misoprostol Options include: 💕Manual vacuum under local anaesthetic 💕Surgical management under general anaesthetic (GA) 💕Nb. Anti-D Ig must be offered to all Rh -ve women who have surgical management of miscarriage.
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Threatened miscarriage
Threatened miscarriage - symptoms (bleeding), but closed cervical os with viable pregnancy, foetal heartbeat present etc. Management: Vaginal progesterone (400mg BD) - continue until 16 completed weeks of pregnancy - may reduce risk of miscarriage If bleeding worsens, lasts > 14 days - repeat assessment.
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Management of Miscarriage If suspected ectopic pregnancy, haemodynamically unstable or concerns about amount of bleeding - admit/ refer to EPAU If > 6 weeks - refer to EPAU
If > 6 weeks - refer to EPAU TVUS to confirm location/viability of pregnancy, and rule out ectopic pregnancy (laparoscopy if suspected) If the pregnancy remains viable, treat as a threatened miscarriage The pregnancy can then be managed with either: Expectant management Medical management Surgical management
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Management of Miscarriage If suspected ectopic pregnancy, haemodynamically unstable or concerns about amount of bleeding - admit/ refer to EPAU If < 6 weeks pregnant and bleeding but NO pain/complications - consider expectant management
Expectant management - allow natural course of miscarriage, and repeat urine pregnancy test in 7-10 days If negative - confirms miscarriage If positive / ongoing bleeding or worsening symptoms - refer to EPAU
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Miscarriage The spontaneous termination of a pregnancy at < 24 weeks gestation Early miscarriage - < 13 weeks Late miscarriage - between 13-24 weeks Terminology Missed miscarriage - foetus is not alive, mother is asymptomatic (no pain, bleeding) Threatened miscarriage - Vaginal bleeding, BUT the cervix remains closed and pregnancy is still viable at present Inevitable miscarriage Vaginal bleeding with open cervical Os - pregnancy is no longer viable - will proceed to incomplete or complete miscarriage Incomplete miscarriage - Foetus no longer alive, products of conception are retained within the uterus Complete miscarriage - products of conception have been completely expelled
Clinical features History of pregnancy OR amenorrhoea/breast tenderness etc. PV Bleeding Lower abdominal pain - often cramping, may radiate into back Investigations Investigation of choice - transvaginal ultrasound Features include absence of foetal heartbeat, or abnormal development (e.g. absent foetal pole)
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Menorrhagia Background Menorrhagia Heavy blood loss during menstruation which affects as woman’s quality of life Causes Idiopathic - 50% Uterine pathology - fibroids, endometrial polyps, endometriosis/adenomyosis Disorders of clotting - VWD, or medications (antiplts/anticoags) Complications The commonest cause of IDA in menstruating women
Investigations Initial investigations Bloods - FBC (?IDA), coagulation screen (?VWD), TFTs HVS/Cervical swab if symptoms of infection Further investigations If symptoms/signs suggest probable underlying pelvic pathology arrange further investigations: Suspected fibroids (palpable uterus/pelvic mass) - pelvic ultrasound Suspected endometrial pathology/submucosal fibroids - hysteroscopy Suspected adenomyosis (dysmenorrhoea, bulky tender uterus) - TVUS
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2WW Referrals 2 week wait referral (via suspected cancer pathway) Pelvic mass with features of malignancy (unintentional weight loss/unexplained bleeding) Age > 55 with post-menopausal bleeding Abnormal cervical examination ?Cervical ca. Ascites and or abdominal mass which is not likely due to fibroids (“urgent referral”)
Management For the following patients Menorrhagia with no identified pathology (previous termed dysfunctional uterine bleeding) Fibroids < 3cm Adenomysosis 1st line: Levonorgestrel intrauterine system (LNG-IUS) Prevents endometrial proliferation 2nd line: If LNG-IUS unsuitable or declined - consider pharmacological treatment: Non-hormonal - either TXA or NSAID (mefenamic acid) Hormonal - COCP/cyclical progestogen For patients with fibroids >3cm Refer to gynaecology - consideration of surgical mx (e.g. myomectomy), uterine artery embolisation, as well as above treatment options.
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Uterine Fibroids (Leiomyomas) Pathophysiology Benign smooth muscle tumours of the myometrium Clinical features Menorrhagia Pressure symptoms: Pelvic pain, dyspaereunia Urinary frequency/urgency Bowel - constipation, bloating Subfertility/infertility (esp. if fibroids are submucosal)
Examination findings An enlarged, firm, irregular uterus (not tender on palpation) An irregular abdominal mass Management Menorrhagia - As per above notes (>3cm - gynae, < 3cm - LNG-IUS) Subfertility/pressure symptoms - refer to gynae Complications: Red degeneration of Fibroids Definition: Ischaemia and subsequent necrosis of a fibroid, which commonly occurs during the second or third trimester of pregnancy, due to disruption of the fibroids blood supply Clinical features: Severe, acute abdominal pain, N&V, low fever - in a pregnant woman with a history of fibroids.
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Menopause & HRT Background The permanent cessation of menstruation, due to the depletion of the oocyte store, and resultant loss of ovarian follicular activity A diagnosis can be made after amenorrhoea for 12 months Early menopause - menopause occurring between ages of 40-45 years Premature menopause - menopause at < 40 years The perimenopause is the time before the menopause, characterised by oligomenorrhea and vasomotor symptoms (hot flushes/night sweats)
Clinical Features A change in menstrual cycle in the perimenopause - e.g. lengthening or shortening of the cycle length Vasomotor symptoms Hot flushes Night sweats Mood disorders Mood swings, anxiety, irritability or low mood Genitourinary syndrome of menopause: Oestrogen deficiency in post-menopausal women causes atrophy of the vaginal lining. Clinical features: vaginal irritation and soreness, commonly worsened by sex Post-coital bleeding - trauma to fragile vaginal skin. Vaginal dryness, itching or discomfort Associated dyspareunia On examination: smooth, pale, dry vaginal walls with contact bleeding. Reduced libido
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Management of Genitourinary Syndrome of Menopause Hormonal
Hormonal 1st Line: Low dose vaginal oestrogen (can also be added to systemic HRT if severe symptom) 2nd line: Trial oral ospemifene (SERM) if mod-severe symptoms. Non-hormonal Vaginal moisturisers
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Non-hormonal alternatives
Vasomotor symptoms SSRI or SNRI - fluoxetine, citalopram, paroxetine, venlafaxine Clonidine (alpha-2 R agonist - also used in rosacea) Gabapentin CBT Mood disorders Antidepressant treatment
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Diagnosis If there are typical symptoms a diagnosis can be made. In some cases, measurement of FSH can aid diagnosis of menopause: Age > 45 with atypical symptoms Possible early menopause - age 40-45 with symptoms as above Age < 40 with suspected premature menopause If the FSH level is > 30 this indicates ovarian insufficiency (2 x samples 6 weeks apart to confirm).
Contraception Inform women that they may remain fertile for up to 2 years after their last menstrual cycle if < 50 years of age (or 1 year if > 50 years of age) and so should continue to use contraception during this… period. Progestogen only contraception can be used alongside cyclical HRT Combined hormonal contraception (e.g.COCP) can be used as an alternative to HRT in women who are < 50 years of age, for the relief of menopausal symptoms (but should switch to progestogen-only contraception once > 50yrs)
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Hormone replacement therapy (HRT) The management of menopause and HRT in particular is a common topic in the MSRA (i.e. which is the most appropriate HRT regimen for X patient? etc.) The most appropriate type of HRT depends on: Uterus or no uterus (hysterectomy) In women without a uterus (hysterectomy) - offer oestrogen only HRT In women with a uterus - offer a combined HRT (oestradiol + progesterone) The progestogen provides endometrial protection - unopposed oestrogen would cause endometrial hyperplasia and increase risk of cancer. Next consider sequential vs continuous combined...
For COMBINED HRT - Timing of LMP Perimenopausal - periods ongoing or stopped < 1 year ago - Sequential (cyclical) combined HRT Oestrogen is taken every day, and the progesterone is taken for aprox. half of the month Results in a monthly withdrawal bleed Post-menopausal - LMP was > 1 year ago - Continuous combined HRT Continuous = oestrogen and progesterone are taken together every day Continuous is preferred - advantage is NO withdrawal bleeding
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To summarise.. Hysterectomy/no uterus - oestrogen only Uterus intact LMP < 1 year ago - sequential combined LMP > 1 year ago - continuous combined Duration of treatment HRT should be continued as long as required until no longer necessary for symptom relief (i.e. the symptomatic benefits are outweighed by risks of HRT). Women with premature menopause/premature ovarian insufficiency should continue HRT until at least age 51 (average age of menopause).
Routes Systemic oestrogen can be taken orally or transdermally (patch, gel, spray) Importanlty, transdermal oestrogen is NOT associated with increased risk of VTE (PO oestrogen only!) Contraindications to HRT (1) Breast/Endometrial Cancer (2) Clots (3) Liver disease (4) Pregnancy History of breast cancer or endometrial cancer By the same logic - undiagnosed breast lump/ PV bleeding/untreated endometrial hyperplasia History of VTE (PE/DVT), thromboembolic disease (angina/MI) or thrombophilic disorder Active liver disease Pregnancy
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Side effects of HRT Oestrogen - breast tenderness, bloating, fluid retention Progestogen - breast tenderness, low mood, acne vulgaris Vaginal bleeding - common within 1st 3/12 especially Continuous combined HRT common SE - irregular bleeding/spotting for 4-6 months Combined hormonal contraception Combined hormonal contraception (e.g.COCP) can be used as an alternative to HRT in women who are < 50 years of age, for the relief of menopausal symptoms
Non-hormonal alternatives Vasomotor symptoms SSRI or SNRI - fluoxetine, citalopram, paroxetine, venlafaxine Clonidine (alpha-2 R agonist - also used in rosacea) Gabapentin CBT Mood disorders Antidepressant treatment
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Meigs Syndrome Meigs syndrome is a rare condition characterised by the triad of benign ovarian fibroma, ascites, and pleural effusion. It is important to differentiate it from malignant conditions. Clinical features Ovarian Fibroma - benign Pelvic mass Ascites Abdominal distension Pleural Effusion SOB
Management Surgical Resection of the ovarian fibroma leads to resolution of ascites and pleural effusion.
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Management of UTI during Pregnancy
Management Send urine MCS 1st line: Nitrofurantoin (avoid at term) 100mg BD for 7 days (if eGFR > 45) 2nd line: Amoxicillin 500mg TDS 7 days, cefalexin 500mg BD 7 days Trimethoprim is contraindicated (folate antagonist) Note - A repeat urine culture should be performed after completion of antibiotic treatment in pregnancy, as a test of cure.
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Infertility Background Various definitions - commonly - the failure to conceive after one or two years of frequent UPSI Sub/infertility is very common - It affects approximately 1/8 couples in the UK Causes Ovulatory disorders Tubal pathology RFs: STIs/PID, endometriosis Male infertility - oligozoospermia (reduced number), asthenozoospermia (impaired motility), teratozoospermia (abnormal morphology) - often occurring together
Causes of infertility Disorders of ovulation The most common cause of infertility in women Causes include: ❤️Hypogonadotropic hypogonadism - usually present with primary or secondary amenorrhoea Stress/exercise/eating disorder induced hypothalamic amenorrhoea Kallman syndrome (clue: anosmia) ❤️Hypothalamic-pituitary-ovarian axis disorders - often present with oligo-/amenorrhea PCOS Hyperprolactinaemic amenorrhea (prolactinoma, drug-induced etc.) ❤️Ovarian failure Suggested by high levels of gonadotrophins (LH/FSH) and low levels of oestrogen ❤️Other: Endocrine (thyroid dysfunction, Cushing’s syndrome, CAH), chronic disease
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Male infertility Causes of male infertility include: Primary spermatogenic failure Testicular dysgenesis, trauma, torsion, tumour etc. Genetic disorders: Klinefelter’s syndrome (47XXY) Kallman syndrome Obstruction of ejaculatory duct, vas deferens etc. Varicocele Drugs - sulfasalazine, steroids
Investigations Investigations should begin after 1 year of failure to conceive for couples who are having regular UPSI every 2-3 days. Consider earlier investigation if: Woman is age > 36 years - begin investigations after 6 months of trying History of oligo-/amenorrhoea History of PID/STI/medical history that might affect fertility in male/female
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Investigations Investigations should begin after 1 year of failure to conceive for couples who are having regular UPSI every 2-3 days. Consider earlier investigation if: Woman is age > 36 years - begin investigations after 6 months of trying History of oligo-/amenorrhoea History of PID/STI/medical history that might affect fertility in male/female
Investigations - Female patient ❤️Mid-luteal phase progesterone - Send for all women! Confirms ovulation Should be taken 7 days before the expected period For a 35 day cycle - measure on day 28 For a 28 day cycle - measure on day 21 ❤️Consider the following Gonadotropins (FSH/LH - usually on D2-D4 of cycle) Low in hypogonadotrophic hypogonadmis (hypothalamic amenorrhoea - XS exercise/weight loss/ED) High in ovarian failure Prolactin, TFTs STI screen ❤️Investigations in secondary care may include: Tubal patency test If no history of comorbidities which may affect tubal patency (PID/endometriosis) - HYSTEROSALPINGOGRAPHY If there is a history - diagnostic laparoscopy and dye - assess tubes and pelvis simultaneously
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Ovarian Hyperstimulation Syndrome (OHSS) A life-threatening complication associated with fertility treatments including clomifene, IVF. Clinical features: Abdominal pain/bloating Nausea and vomiting Severe OHSS is suggested by: Oliguria Oedema Ascites Thromboembolism Hydrothorax
Initial investigations - Male patient Semen analysis Consider STI screen Management options.. Medical - clomifene, gonadotrophins Surgical management - e.g. if tubal abnormalities/endometriosis Assisted conception - IUI/IVF/ICSI etc.
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Antepartum Haemorrhage Background Antepartum haemorrhage - Bleeding from the genital tract from 24 weeks of pregnancy until birth Important causes of APH include: Placental abruption Placenta praevia Vasa praevia
Placental Abruption Pathophysiology The separation of part, or all of the placenta from the wall of the uterus during pregnancy with resultant antepartum haemorrhage. Bleeding can be: Revealed - Blood tracks down genital tract - visible APH Concealed - Cervical os remains closed, bleeding remains in uterine cavity- presenting with abdominal pain and shock Risk factors History of P. abruption, pre-eclampsia, multiple pregnancy, increasing age, smoking
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Severity Spotting Minor - < 50ml blood loss Major - 50ml-1L blood loss Massive - > 1L Blood loss OR signs of shock Clinical Assessment Symptoms Sudden onset, severe and continuous abdominal pain Antepartum haemorrhage - PV bleeding Examination findings A tender, firm, ‘woody’ uterus on palpation Haemodynamic compromise/shock - tachycardia, hypotension
Investigations Diagnosis is clinical, though US can be used to diagnose placenta praevia CTG monitoring should be performed Management Maternal resuscitation and blood transfusion is required Foetal management: If there is foetal distress, urgent c-section should be considered If no foetal distress and > 37 weeks gestation - induction of labour < 37 weeks gestation - admit, give steroids if required for foetal lung maturation
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Placenta Praevia Pathophysiology Terminology: Placenta praevia (PP) - the placenta is attached to the lower portion of the uterus and lies directly over the internal cervical os Low lying placenta (LLP) - where the internal cervical os is NOT covered, but the placenta is within 20mm. Risk Factors: Previous c-section, fibroids Investigations Transvaginal ultrasound is the diagnostic investigation of choice Clinical features Painless, visible vaginal bleeding, usually occurring late in pregnancy (often > 35 weeks).
Management Monitoring: If PP or LLP is identified at the routine foetal anomaly scan (20 weeks), a follow up TVUS is recommended at 32 weeks to diagnose persistent LLP /PP. If there is evidence of persistent LLP or PP, an additional TVUS should be performed at 36 weeks as this will inform the most appropriate mode of delivery Corticosteroids are given to aid fetal lung maturation, due to the increased risk of prematurity Patients with PP require planned c-section at 36-37 weeks to reduce the risk of severe bleeding.
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Vasa Praevia Pathophysiology The foetal blood vessels (umbilical arteries and vein) are exposed, and travel across or run near to the internal os of the uterus. They are at risk of bleeding, particularly when there is rupture of membranes during labour. Clinical features Symptoms Antepartum haemorrhage Bleeding following rupture of membranes, with associated foetal distress - high risk of foetal mortality Triad: Membrane rupture, painless vaginal bleeding, fetal distress/bradycardia
Management Planned, c-section at 34-36 weeks (to avoid spontaneous rupture of membranes) Corticosteroids for foetal lung maturation
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Asherman's Syndrome Pathophysiology The formation of adhesions within the uterus, which form as a result of trauma to the endometrium. Causes include dilatation and curettage procedures (e.g. for removal of retained products), uterine myomectomy, or endometritis. Adhesions lead to partial or complete obliteration of the uterine cavity, causing obstructions and distortion, with resultant infertility, miscarriage, abnormalities in menstruation (dysmenorrhoea, amenorrhoea)
Investigations Hysteroscopy - the gold standard Management Surgical dissection of adhesions during hysteroscopy, often combined with placement of intrauterine devices or barriers to prevent adhesion reformation.
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Atrophic Vaginitis Key learning Due to decreased oestrogen levels- > thin and inflamed vaginal walls-> less lubrication-> increased susceptibility to infection Most common in post menopausal Examination: Dry, pale, atrophic vagina Management: 1st line: Vaginal lubricants 2nd line: Topical oestrogen therapy Pathophysiology Decreased oestrogen levels, leading to thinning and inflammation of the vaginal walls Results in reduced lubrication Increased susceptibility to infection Risk factors
Risk factors Postmenopausal women due to oestrogen deficiency Premenopausal women during breastfeeding Patients undergoing chemotherapy or hormonal therapy History Vaginal dryness, itching, burning Dyspareunia (painful intercourse) Occasional spotting Urinary symptoms such as frequency or urgency Examination Findings Vaginal mucosa appears pale, dry, and atrophic May have petechiae or ulceration Investigations Clinical diagnosis Vaginal pH may be elevated (>5) Hormonal assays may be indicated in certain cases to evaluate oestrogen levels. Management 1st line- Vaginal moisturizers, and lubricants 2nd line- Topical oestrogen therapy (cream, ring, or tablet) Complications Recurrent urinary tract infections Vaginal or urethral prolapse Sexual dysfunction
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Bartholin's Cyst Bartholin's cysts are fluid-filled swellings that occur when the duct of the Bartholin's gland becomes obstructed. The Bartholin's glands, located bilaterally at the posterior introitus (at 4 o’clock and 8 o’clock of the vulva), secrete mucus to lubricate the vaginal mucosa, maintaining the moisture of the vaginal mucosa, and facilitating intercourse. Pathophysiology The Bartholin's glands secrete mucus through ducts that open at the vaginal introitus. These secretions help lubricate the vaginal mucosa, facilitating sexual intercourse. When the ducts become obstructed, mucus accumulates, leading to the formation of a cyst. If the cyst becomes infected, an abscess can develop, causing significant pain and swelling.
Clinical Features Asymptomatic swelling - Small cysts may be asymptomatic and discovered incidentally . Classically a unilateral swelling at 4 / 8 o’clock, on the inferior labia majora, which protrudes medially Pain - Larger cysts can cause significant pain, especially during walking, sitting, or sexual intercourse. Dyspareunia: Painful intercourse due to the cyst's location near the vaginal opening. Bartholin's abscess - present with erythema, marked tenderness and sometimes fever.
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Mng bartholin cyst
Management Conservative management may be considered if asymptomatic. Medical Management: Antibiotics - if evidence of infected cysts / abscesses. Surgical Management: Incision and Drainage: For symptomatic or infected cysts/abscesses. Word Catheter: Inserted after drainage to allow continued drainage and prevent recurrence. Marsupialisation: Creation of a permanent opening to prevent future cyst formation, typically reserved for recurrent cases.
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Caput Succedaneum Pathophysiology: Caused by pressure on the foetal head against the cervix during labor, leading to oedema in the scalp's subcutaneous tissue. Clinical Features: Swelling of the soft tissues of the scalp, outside of the periosteum Crosses suture lines Present at birth Soft, pitting oedema Resolves within a few days
Cephalohaematoma Pathophysiology: Caused by rupture of blood vessels crossing the periosteum due to trauma during delivery, leading to blood accumulation. Clinical Features: Collection of blood between the periosteum and skull bone Does NOT cross suture lines Typically appears hours to days after birth Firm, well-defined edges Takes weeks to months to resolve Key Points Caput succedaneum is soft and crosses sutures, while cephalohaematoma is firm and does not cross sutures. Caput resolves quickly, whereas cephalohaematoma takes longer and may lead to complications like jaundice or infection.
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Breast Cancer Breast cancer is the most common cancer in women Classification Non-invasive breast cancer - cancer cells have not invaded the basement membrane. They are commonly referred to as pre-malignant, and are at risk of progression into invasive breast cancer. Ductal carcinoma in situ (DCIS) - arise from the epithelial cells which line the breast ducts Lobular carcinoma in situ (LCIS) - arise from the epithelial cells within the breast lobules Invasive breast cancer Invasive ductal carcinoma - most common Invasive lobular carcinoma
Other, rare types of breast cancer include Paget’s disease of the nipple Erythematous, dry, scaly ulceration of the skin around the nipple. Sore, itchy. Significance: Paget’s is usually associated with an underlying breast malignancy (in situ or invasive). Inflammatory breast cancer Rare and aggressive breast malignancy which results from lymphatic obstruction by malignant cells. The breast becomes painful, erythematous and oedematous.
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Risk factors Genetics - BRCA1/2 = 40% lifetime risk of breast or ovarian carcinoma Family history Menstrual risk - early menarche, late menopause Pregnancy and breastfeeding are protective! So nulliparity/late 1st pregnancy (>30yrs) are RFs Oestrogen containing medications: combined HRT, COCP
Clinical Features Breast lump A painless breast lump is the most common presenting complaint On examination, malignant lumps may feel hard or ‘gritty’, with irregular margins. Due to their invasive nature they may also be fixed to the chest wall or tethered to surrounding tissue. Axillary lymphadenopathy Nipple changes Paget’s disease - erythematous, ulcerated skin around nipple Change in shape, colour Irritation or bleeding Discharge and retraction Skin changes Dimpling, puckering of skin Peau d’orange
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Breast ca Referral Refer via a 2WW suspected cancer pathway if: Unexplained axillary lump and age > 30 Age > 30 and Breast lump (regardless of painful/painless) If age < 30 and breast lump, consider non-urgent referral Age > 50 and unilateral nipple changes Skin changes suggestive of breast malignancy (Peau d’orange) Assessment Following referral, patients undergo a triple assessment 💕History/Examination 💕Imaging Ultrasound in younger patients (<40) due to denser breast tissue making mammography less sensitive Mamogram in women > 40 with two views 💕Biopsy - core biopsy/FNA
Management Patients may be managed with a combination of chemotherapy (neoadjuvant or adjuvant), radiotherapy, and surgery (wide local excision, mastectomy) with sentinel node sampling to identify lymph node involvement. Pharmacological treatments include Anti-oestrogen therapy - to reduce oestrogen dependent tumour growth Tamoxifen - ER blocker - used in premenopausal women with ER+ BC SEs: Flushes, VTE risk, menstrual cycle disturbance Typically continued for up to 5 years post-excision Aromatase inhibitors (anastrozole, letrozole etc) - used in postmenopausal women with ER+ BC (blocks the conversion of androgens into oestrogen). Biological treatments Herceptin (trastuzumab) - monoclonal antibody used in HER2+ BC.
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Screening and Family History Managing Family History of Breast Cancer NICE advises that the following cohorts of patients should be offered referral for specialist assessment on the basis of family history: One first-degree female relative with BC < 40 yrs One first-degree male relative with BC at any age One first-degree relative with bilateral breast cancer (where first BC was Dx at < 50 yrs) One relative with BC and one with ovarian ca at any age Three 1st/2nd degree relatives with BC at any age
The NHS Breast Screening Program Women aged 50-70 years 3-yearly routine breast screening which uses mammography to detect breast cancer Differential diagnosis 💕Breast cyst Smooth, fluid-filled lump, may be painful Size varies throughout menstrual cycle 💕Fibroadenoma Common in young patients (20-30) Discrete, rubbery, firm and non tender Highly mobile, so sometimes referred to as “breast mouse” ❤️Fat necrosis A fibrotic lump which occurs following trauma to the breast More common in obese women 💕Breast abscess A painful, inflamed lump with systemic upset such as fever, malaise, SIRS Commonly occurs during breastfeeding Examination - erythematous, warm and tender to touch 💕Cyclical breast pain Hormone related breast pain - presents with pain which starts within 2 weeks of menstruation, gradually increases and then improves once period begins Pain is usually bilateral Management - simple analgesia (paracetamol +/- ibuprofen)
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Breech presentation Definition and Types Breech presentation is when the foetus is positioned with the buttocks or feet closest to the cervix. It occurs in approximately 3-4% of full-term pregnancies and is more common in preterm deliveries. Subtypes include: Frank breech: hips flexed, knees extended (most common). Complete breech: hips and knees flexed. Footling breech: one or both feet presenting first. Clinical Presentation Diagnosis is typically made during routine prenatal examinations through palpation and confirmed by ultrasound. The presence of foetal buttocks or feet in the maternal pelvis can indicate breech presentation.
Management Management depends on factors including gestational age, type of breech, and maternal preference. Breech at < 36 weeks gestation: Often resolves spontaneously due to the space available in the uterus. Therefore, no intervention is typically recommended at this stage. Breech at > 36 weeks in nulliparous women or > 37 weeks in multiparous women: External cephalic version (ECV) is offered to attempt to turn the foetus to a cephalic (head-first) position. ECV involves applying gentle pressure on the pregnant abdomen to manually rotate the foetus. The success rate is approximately 60%. Failed ECV: If ECV is unsuccessful, a decision needs to be made between attempting a vaginal delivery (which is generally safer for the mother) or opting for a planned caesarean section (which is generally safer for the baby in breech presentations). Anti-D prophylaxis: If the mother is rhesus-negative and undergoes ECV, it is considered an indication for anti-D prophylaxis to prevent rhesus isoimmunisation, where maternal antibodies attack foetal red blood cells. This is a standard practice to prevent sensitisation in subsequent pregnancies. Complications Complications of breech delivery include foetal head entrapment, umbilical cord prolapse, birth trauma (such as brachial plexus injury), and perinatal asphyxia
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Cervical Cancer Pathophysiology Most cases of cervical cancer arise from the ecto- or endocervical mucosa 80% are squamous cell carcinoma The primary cause if HPV (16 & 18) infection which induces cellular dysplasia Clinical features Most commonly affects sexually active women aged 30-45 Unexplained vaginal bleeding - e.g. intermenstrual, post-coital etc. Unexplained abnormal vaginal discharge (can be bloody) which is not secondary to infection Dyspareunia Pelvic pain Abnormal cervical appearance - e.g. inflamed, presence of contact bleeding, or visible lesion
Screening program Inclusion: Women aged 25-64 years Cervical smear every 3 years from ages 25-49 Cervical smear every 5 years from ages 50-64 Unscheduled cervical screening: Not recommended if the previous smear test is up to date. Women with new symptoms should be referred to gynaecology. If a cervical smear is postponed due to pregnancy it should be performed 12 weeks after delivery. Referral Refer any women with clinical features suggestive of cervical cancer (as above) using a 2 week wait referral via a suspected cancer pathway, for urgent colposcopy/specialist assessment, regardless of previous screening results.
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Infections During Pregnancy Rubella in Pregnancy Rubella can cause serious complications in pregnancy - importantly, congenital rubella syndrome (the risk of which is greatest if rubella is contracted in the first 20 weeks of gestation). RFs: Incomplete immunisation Clinical features Develop 2 or 3 weeks post exposure.. Rash - A pink/ light red rash which starts on face and neck, and then spreads to rest of body Lymphadenopathy Arthralgia Low grade fever, malaise, URTI symptoms etc.
Congenital rubella syndrome Sensorineural hearing loss Cataracts, chorioretinitis (with “salt and pepper” retinal appearance) Congenital heart disease - Patent ductus arteriosus CNS - microcephaly Hepatosplenomegaly Blue muffin rash Assessment and Management Contact health protection team immediately, notifiable disease IgG -ve women should keep take precautions to avoid exposure, offer vaccine post-natal IgM +ve confirms recent exposure If rubella confirmed, refer to O&G If 8-10 weeks gestation, 90% risk of CRS, and no effective treatments If > 20 weeks - reassure
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Varicella Zoster Virus in Pregnancy Prevention of varicella in pregnant women with exposure: Step 1: Take a careful history to assess exposure and patient susceptibility. Step 2: Blood test recommended for women with uncertain history or from tropical/subtropical countries to check VZV immunity. If VZ IgG positive - confirms immunity - reassure patient, no further management required. If VZ IgG negative - non-immune - manage as below If non-immune and significant exposure: 1st Line: Offer Post Exposure Prophylaxis (PEP) with oral antivirals (aciclovir/valaciclovir) from Day 7 to 14 post-exposure (Updated 2024) If PO antivirals are contraindicated, consider VZIG for PEP, effective up to 10 days post-exposure.
Care for pregnant women who develop chickenpox: 1st Line: Prescribe oral aciclovir if presenting within 24 hours of rash onset if 20+0 weeks of gestation or beyond (should also be "considered" if < 20 weeks gestation) Aciclovir/valaciclovir can be used in pregnancy, based on evidence and consultation, despite not being licensed for this use, in patients best interest. Severe chickenpox - Intravenous aciclovir recommended for all severe cases. VZIG NOT beneficial once chickenpox rash develops. Referral and follow-up: Refer to a foetal medicine specialist at 16–20 weeks or 5 weeks post-infection for detailed ultrasound. Discuss risks/benefits of amniocentesis for detecting varicella DNA via PCR, with awareness of predictive limitations. Avoid amniocentesis until after skin lesions heal.
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Congenital toxoplasmosis
Congenital toxoplasmosis Clinical Features Chorioretinitis Hydrocephalus Intracranial calcification
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Congenital cytomegalovirus
Congenital cytomegalovirus Clinical features Growth restriction Microcephaly and learning disability Sensorineural hearing loss Loss of vision Seizures
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Induction of Labour Indications for Induction of Labour (IOL) Induction of labour is warranted when continuing the pregnancy poses risks to the mother or foetus, or when the benefits of delivery outweigh those of continuing the pregnancy. Common indications include: Post-term pregnancy without spontaneous labour (usually offered at between 41-42 weeks gestation). Pre-labour rupture of membranes (PROM) Gestational hypertension Foetal growth restriction Maternal medical conditions such as diabetes or pre-eclampsia.
Bishop Score The Bishop score can be used to predict whether IOL will be successful. It assesses cervical readiness for labour induction based on cervical dilation, effacement, station, consistency, and position. A score of 6 or less indicates an unfavourable cervix, whereas a score higher than 6 suggests a favourable cervix for induction. Strategies for Induction of Labour 💕Membrane Sweep: Inserting a finger into the cervix to separate the amniotic membranes from the lower uterine segment. Stimulates prostaglandin release, which can initiate labour within 48 hours. 💕Dinoprostone (Prostaglandin E2) Indicated in women with an unfavourable cervix (Bishop Score ≤6). Administered as vaginal gel, tablet, or slow-release pessary to soften the cervix. 💕Amniotomy (Artificial Rupture of Membranes - ARM) followed by IV Oxytocin Infusion Recommended for women with a favourable cervix (Bishop Score >6). 💕ARM involves deliberate breaking of the amniotic sac followed by IV oxytocin infusion to stimulate uterine contractions. ❤️Complications Potential complications include Uterine hyperstimulation Foetal distress Increased risk of instrumental delivery or caesarean section.
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Incontinence Stress incontinence The involuntary passage of urine associated with raised intra-abdominal pressure (e.g. on sneezing, coughing, laughing). Cause/RFs: Pelvic floor muscle weakness - age, pregnancy and vaginal delivery, obesity, constipation Management Step 1: Supervised pelvic floor muscle training Step 2: Refer to urogynaecology for consideration of surgical mx Duloxetine - If the woman would prefer drug treatment than surgical mx - offer duloxetine as a 2nd line treatment
Urgency incontinence A sudden sense of the need to pass urine, followed by incontinence Usually idiopathic - part of OAB syndrome, characterised by the presence of urgency, frequency, nocturia (which occur due to involuntary detrusor muscle contractions) Management Step 1: Bladder training (minimum 6 weeks) Step 2: If ongoing symptoms, consider either: Antimuscarinic (oxybutynin, tolterodine, darifenacin) Avoid oxybutynin in older women at risk of deterioration of mental or physical health - high risk adverse effects and cognitive impairment Mirabegron (beta-3 agonist) - if antimuscarinic is contraindicated
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Mixed incontinence and overflow incontinence
Mixed incontinence A combination of stress and urgency incontinence Management: follow above management for the most pressing symptom (i.e. stress vs urgency) Overflow incontinence Urinary retention occurs due to bladder outflow obstruction (BOO) or detrusor muscle dysfunction, which is followed by involuntary ‘overflow’ leakage. Management: Refer to specialist
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Hypothyroidism in Pregnancy Physiology In pregnancy, there is an increase in TBG (thyroid binding globulin) This results in an increase in the TOTAL T4 Note - the level of FREE T4 remains the same Monitoring Measure TSH every trimester and 8 weeks postpartum
Levothyroxine Levothyroxine is safe in pregnancy and breastfeeding patients Pregnant patients often require significantly increased doses of levothyroxine Current guidance states that in a woman with known stable hypothyroidism who becomes pregnant, immediately increase the levothyroxine dose (an increase of 30-50% is commonly required) Typically, increase the dose of levothyroxine by least 25–50 micrograms levothyroxine (depending on dose the woman is currently taking). For example, for a woman with stable hypothyroidism on 125 mcg of levothyroxine OD, who becomes newly pregnant, increase the dose to 175 mcg levothyroxine OD To avoid delay, increase the dose before checking TFTs If there is uncertainty about what dose to prescribe, seek specialist advice promptly to avoid delay.
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Hypertension in Pregnancy A common complication, associated with serious implications for both mother and foetus if uncontrolled. Blood pressure normally decreases in the first trimester, then increases. Diagnosis of Hypertension in Pregnancy Hypertension is diagnosed in pregnancy if ANY of the following occurs: Blood pressure > 140/90 (either systolic/diastolic) Systolic BP increases by 30mmHg or more Diastolic BP increases by 15mmHg or more
Classification of Hypertension Patients with hypertension should be categorised into: (1) Pre-existing hypertension A previous diagnosis of hypertension OR Hypertension is diagnosed before 20 weeks gestation (2) Pregnancy Induced Hypertension Hypertension diagnosed after 20 weeks gestation Usually resolves following delivery, increased future risk of pre-eclampsia ( 3) Pre-eclampsia Hypertension AND Proteinuria (>0.3g/24hrs) Patients may develop oedema
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Risk factors for Pre-eclampsia
❤️High risk Prescribe all patients with high risk aspirin 75-150 mg OD from 12 weeks until birth Hypertension in a previous pregnancy Pre-existing diagnosis of hypertension Background of autoimmune disease including SLE & antiphospholipid syndrome Chronic kidney disease (CKD) Diabetes (T1 & T2) ❤️Moderate risk Prescribe patients with 2 of the following RFs aspirin as above. 1st pregnancy Age > 40 Pregnancy interval longer than 10 yrs BMI > 35 FHx of pre-eclampsia Multiple pregnancy
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Complications of Pre-eclampsia Foetal: Prematurity, IUGR, Placental abruption Maternal: Heart failure, Haemorrhage – abdominal or cerebral, Multi-organ failure, Eclampsia Severe Pre-eclampsia Pre-eclampsia is diagnosed in the presence of hypertension AND PROTEINURIA (>0.3g/24hrs). Associated with high risk of eclampsia. Pre-eclampsia is classified as severe in the presence of any of the following: Severe hypertension – BP >170/110 (systolic or diastolic) Significant proteinuria – dipstick ++ or +++ Clinical features Headache RUQ or epigastric pain Visual disturbance Hyperreflexia Papilloedema Bloods: Platelets < 100 Deranged LFTs HELLP syndrome
Complications of Pre-eclampsia Foetal: Prematurity, IUGR, Placental abruption Maternal: Heart failure, Haemorrhage – abdominal or cerebral, Multi-organ failure, Eclampsia Severe Pre-eclampsia Pre-eclampsia is diagnosed in the presence of hypertension AND PROTEINURIA (>0.3g/24hrs). Associated with high risk of eclampsia. Pre-eclampsia is classified as severe in the presence of any of the following: Severe hypertension – BP >170/110 (systolic or diastolic) Significant proteinuria – dipstick ++ or +++ Clinical features Headache RUQ or epigastric pain Visual disturbance Hyperreflexia Papilloedema Bloods: Platelets < 100 Deranged LFTs HELLP syndrome
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Management of Pre-eclampsia The only cure for pre-eclampsia is delivery Management until delivery includes: Aspirin 75-150 mg OD Anti-hypertensive medications: IF BP > 160/110 1st Line: Oral Labetalol Alternatives: Nifedipine, hydralazine Severe pre-eclampsia – Magnesium (same as for eclampsia below
Eclampsia Eclampsia is defined as seizures developing in the context of pre-eclampsia Management: magnesium sulfate - 4g bolus, followed by 1g/hour infusion HELLP Syndrome A complication defined by: Haemolytic anaemia Elevated Liver enzymes Low Platelets
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Hyperemesis Gravidarum Hyperemesis gravidarum is a severe form of nausea and vomiting in pregnancy, leading to significant maternal morbidity. The exact cause of hyperemesis gravidarum is not fully understood, but it is believed to be related to high levels of human chorionic gonadotropin (hCG) and oestrogen. Clinical Features Protracted nausea and vomiting - Persistent and severe, beyond typical morning sickness, in the presence of: Weight loss: 5% or more of pre-pregnancy body weight. Electrolyte derangement - hypokalemia, hyponatremia. Dehydration: dry mucous membranes, decreased skin turgor, and concentrated urine.
Management 1st Line: Promethazine Cyclizine Prochlorperazine Alternatives: Metoclopramide, ondansetron. Additional Measures: Hydration: Oral or IV fluids to correct dehydration and electrolyte imbalances. Nutritional Support: Thiamine/Pabrinex
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Clinical Features of Hydrops Fetalis Skin oedema (>5 mm thick) Pleural/pericardial effusions Ascites Polyhydramnios (excessive amniotic fluid) Placental thickening Elevated MCA peak systolic velocity (MCA-PSV) → Suggests foetal anaemia.
Hydrops Fetalis Overview Hydrops fetalis is a serious foetal condition characterised by abnormal fluid accumulation in two or more foetal compartments, including ascites, pleural effusion, pericardial effusion, and subcutaneous edema. It is an end-stage manifestation of various underlying conditions, leading to severe foetal anaemia, heart failure, and hypoxia. Hydrops is classified into: Immune hydrops – Due to Rhesus (Rh) incompatibility and other alloimmune hemolytic diseases. Non-immune hydrops (NIHF) – Accounts for >85% of cases, caused by a variety of genetic, hematologic, cardiac, infectious, and metabolic conditions. Key learning: 1. Most hydrops is non-immune (>85%) – Think thalassemia, parvovirus, cardiac causes first. 2. Look for clues – Ethnicity, maternal infection, family history, previous losses. 3. MCA Doppler is key to detecting foetal anaemia early. 4. Intrauterine transfusion is lifesaving in severe foetal anaemia. 5. Rh disease is preventable – Always give anti-D immunoglobulin to Rh-negative mothers.
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Hydrops Fetalis Causes
Causes 1. Immune Causes (Alloimmune Haemolysis) Rh incompatibility – Most common immune cause. Clue: Rh-negative mother, second pregnancy, no anti-D prophylaxis. Mechanism: Maternal anti-D antibodies attack foetal Rh-positive red blood cells, causing severe foetal anaemia and resultant hydrops. 2. Non-Immune Causes (Most Common) Hematologic Causes Alpha Thalassemia (Hb Barts Hydrops Fetalis) Clue: Southeast Asian descent, recurrent early hydrops, no alloimmunisation. Mechanism: Absence of functional alpha-globin chains causes severe fetal anemia, hypoxia, and heart failure. Cardiac Causes Congenital Heart Disease Clue: Foetal bradycardia/tachycardia, abnormal echocardiogram. Parvovirus B19 Infection Clue: Contact with a child with “slapped cheek” rash. Mechanism: Virus destroys foetal erythroid precursors, leading to aplastic anaemia and hydrops. Other Infectious Causes (TORCH Infections) Cytomegalovirus (CMV), Toxoplasmosis, Syphilis, Herpes, Rubella Clue: Maternal history of flu-like symptoms, hepatosplenomegaly, intracranial calcifications. Chromosomal & Genetic Causes Turner Syndrome (45,X) & Noonan Syndrome Mechanism: Lymphatic dysplasia leads to fluid accumulation.
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Group B Streptococcus (GBS) in Pregnancy Group B Streptococcus (GBS) is a common bacterium found in the vagina and rectum of 20-40% of women in the UK. While typically harmless, GBS can cause serious neonatal infections such as sepsis, pneumonia, and meningitis. Detection GBS screening is not routinely offered to all pregnant women in the UK. It is often detected incidentally during tests for other reasons, such as urine cultures or vaginal/rectal swabs. Risk Factors for Neonatal GBS Infection Preterm birth (before 37 weeks) Maternal fever during labor Prolonged rupture of membranes (over 24 hours before birth) Positive GBS culture in current pregnancy (urine or swab) Previous baby affected by GBS infection
Management Positive GBS Culture: For any patient with positive GBS in urine/swabs (or previous babies affected by GBS), IV antibiotics should be administered during labor to reduce vertical transmission risk. Antibiotics should be administered as soon as labour begins or membranes rupture, and continued every 4 hours until delivery. Benzylpenicillin is typically 1st line. Asymptomatic Bacteriuria (>10^5): Pregnant women with GBS bacteriuria (>10^5) should receive antibiotic treatment (usually PO amoxicillin) at the time of diagnosis, as well as IV antibiotics during labour (as above) References
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Gestational Trophoblastic disease Gestational trophoblastic disease (GTD) encompasses a spectrum of conditions arising from abnormal proliferation of trophoblastic cells, which normally form the placenta during pregnancy. GTD results from abnormal fertilisation events, typically with excessive paternal genetic contribution or absence of maternal genetic material. The spectrum of GTD includes: Hydatidiform mole (complete and partial) Invasive mole Choriocarcinoma Placental site trophoblastic tumor. Clinical Features Gestational trophoblastic disease (GTD) typically presents in the first trimester of pregnancy. Most cases are diagnosed at 6-12 weeks, due to symptoms such as abnormal vaginal bleeding, enlarged uterus, and elevated serum beta-hCG levels. Clinical presentation varies depending on the specific subtype of GTD. Common features include: Irregular vaginal bleeding from spotting to heavy bleeding. Enlarged uterus: Beyond expected size for gestational age. Hyperemesis gravidarum
Investigations Ultrasound: Characteristic features of molar pregnancy, include the "snowstorm" or "bunch of grapes" appearance (numerous small cystic spaces within the uterus). Elevated serum beta-hCG - often significantly higher than normal pregnancy levels. Histopathology: Confirmation of diagnosis through examination of tissue obtained from dilation and curettage (D&C) or biopsy, revealing hydropic villi with trophoblastic hyperplasia. Management Treatments include evacuation of the molar pregnancy, followed by monitoring serum beta-hCG levels until normalisation. Chemotherapy is tailored based on risk for invasive mole or choriocarcinoma. Surgical resection may be necessary for placental site trophoblastic tumour. Regular follow-up with beta-hCG monitoring and imaging detects recurrence/metastasis.
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Foetal Alcohol Syndrome Pathophysiology Caused by chronic alcohol consumption during pregnancy, which disrupts normal foetal development, particularly in the brain and facial structures. Clinical Features Microcephaly (small head size) Facial abnormalities: Short palpebral fissures, epicanthal folds, low nasal bridge, thin upper lip, indistinct philtrum Low-set or abnormally shaped ears Growth retardation (prenatal and postnatal) Neurodevelopmental issues: Learning disabilities, cognitive deficits, attention problems, and behavioural disorders
Management Early diagnosis and referral for developmental support (e.g., speech therapy, special education) Multidisciplinary approach for managing cognitive, behavioural , and physical complications Preventative: Public health measures to educate on the dangers of alcohol consumption during pregnancy
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Complications of Pregnancy Venous Thromboembolism Treatment 1st Line: subcutaneous LMWH – enoxaparin etc.
Venous Thromboembolism Pregnancy is a hypercoagulable state which results in an increased risk of DVT/PE. Pathophysiology: Increased clotting factors 7, 8, 10 + fibrinogen, decreased protein S levels, increased venous stasis due to uterine compression of the IVC. Investigations + Management Do NOT check D-dimer- raised in pregnancy. Investigating suspected DVT 1st Line: compression duplex US of affected leg Investigating suspected PE If patient also has symptoms of a DVT, perform duplex US first If positive, treat and most patients will not require CTPA or V/Q If no symptoms of DVT, but suspected PE consider CTPA or V/Q after discussion with patient. CTPA – increased risk of breast cancer (approx. 10% increase) V/Q – increased risk of childhood cancer
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Thyroid Problems During Pregnancy Management of Thyrotoxicosis in pregnancy NICE guidelines: Management of thyrotoxicosis during pregnancy Use propylthiouracil in the 1st trimester As carbimazole is associated with increased risk of congenital malformations than PTU is in the first trimester Switch to carbimazole in the 2nd & 3rd trimester As PTU is associated with an increased risk of hepatotoxicity in the 2nd/3rd trimesters Aim to maintain maternal thyroxine levels within the upper 1/3rd of normal
Management of Hypothyroidism in pregnancy Monitoring: Check TSH levels every trimester and at 6-8 weeks post-partum Management: During pregnancy, patients can require a significant increase in levothyroxine dose - typically 50%
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Biliary Problems in Pregnancy Obstetric cholestasis (intrahepatic cholestasis of pregnancy) Timing: Typically third trimester Diagnosis: Consider ICP in pregnant women with pruritus and elevated bile acid concentration ≥19 µmol/L. Clinical Features: Itching - Generalised pruritus (esp of palms of hands/soles of feet) Jaundice, dark urine Complications: Risk of stillbirth & planned delivery Mild ICP (bile acids 19–39 µmol/L): Background stillbirth risk; consider planned birth by 40 weeks. ❤️Moderate ICP (bile acids 40–99 µmol/L): Increased stillbirth risk after 38 weeks; consider delivery at 38–39 weeks. ❤️Severe ICP (bile acids ≥100 µmol/L): Higher stillbirth risk; consider delivery at 35–36 weeks.
Management: No treatments have been shown to reduce adverse perinatal outcomes or bile acid levels. Ursodeoxycholic acid should not be routinely offered for preventing adverse outcomes. Treatment for maternal itching is limited in efficacy - emolients, chlorphenamine may help References: RCOG. Intrahepatic cholestasis of pregnancy (Green-top Guideline No. 43). August 2022. Available at URL: https://obgyn.onlinelibrary.wi...
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Acute fatty liver of Pregnancy AFLOP is another complication of pregnancy, differentiated from OC by its acute presentation and hepatitis picture. Pathology: Rapid accumulation of fat within hepatocytes causing acute hepatitis, with risk of liver failure. Timeline: Most common in 3rd trimester
Clinical Features: Abdominal pain Nausea & vomiting Jaundice Ascites (note HELLP syndrome is more likely if there is thrombocytopenia) Bloods: Hepatitis - ALT often > 500 Management: Delivery
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Polymorphic eruption of pregnancy
Rashes in Pregnancy Polymorphic Eruption of Pregnancy Clinical features An intensely itchy rash which usually begins in the third trimester The rash usually begins on the abdomen (particularly within the abdominal striae) as small, pink papules, often with surrounding pallor. Later the papules coalesce to form urticarial/erythematous plaques Later may spread across the trunk and proximal limbs Resolves following delivery Management Symptomatic relief with antihistamines, topical corticosteroids (or oral if very severe)
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Pemphigoid Gestationis Pathophysiology An autoimmune, blistering rash of pregnancy An IgG autoantibody (called PG factor) develops and targets BP-180 proteins within the basement membrane between the epidermis and dermis
Clinical features Timing: 2nd or 3rd trimesters Intensely itchy, urticarial rash which begins as red bumps, classically around the umbilicus. The rash later spreads acoss the abdomen, and may spread across the trunk, buttocks and limbs. After a few weeks, the lesions develop into tense, fluid-filled blisters Management Topical corticosteroids in mild disease, systemic if severe disease
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Contraception Methods of contraception Barrier - condoms Combined hormonal contraception (CHC) - COCP, combined transdermal patch Progestogen only - POP, implant, injectable Long-acting reversible contraceptives (LARCs) Highly effective contraception, as not dependent on user compliance LARCs include: Intrauterine contraception Levonorgestrel IUS (mirena) Copper IUD Progestogen-only implant
NICE advises to offer whichever method of contraception is preferred by the woman, unless CId. Adverse Effects Levonorgestrel IUS 1/20 risk of expulsion Hormonal side effects - acne, breast tenderness, mood changes Pelvic pain, cramping Irregular periods/Amenorrhoea - periods become irregular, or stop altogether Copper IUD Expulsion 1/20 Pelvic pain, cramping Bleeding - Menorrhagia, intermenstrual bleeding and dysmenorrhoea Progestogen-only implant (e.g. Nexplanon subdermal implant) Unscheduled bleeding, irregular, heavy Reduced efficacy with enzyme inducers
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Contraindications A full list of UKMEC 4 (contraindicated) and UKMEC 3 (risks>benefits) can be viewed at the following: https://www.fsrh.org/standards-and-guidance/documents/ukmec-2016/ Combined hormonal contraceptives - contraindications Some of the most common UKMEC 4 criteria for combined hormonal contraception include: Postpartum Breastfeeding and < 6 weeks postpartum < 3 weeks postpartum with RFs for VTE Past-medical history: Uncontrolled HTN (> 160/100mmHg) Vascular disease History of ischaemic heart disease, AF, heart failure or stroke/TIA History of VTE Major surgery with prolonged immobilisation Migraine with aura Genetics: Breast cancer, or carrier of BRCA1/2 or known thrombogenic mutation Smoking: Age > 35 and smokes > 15/day
Intrauterine device - contraindications Both the Cu-IUD and LNG-IUS are contraindicated in the following: Unexplained vaginal bleeding Current pelvic inflammatory disease or STI (chlamydia/ gonorrhoea) Postpartum sepsis Unexplained PV bleeding UKMEC 4 - Cu-IUD, LNG-IUS UKMEC 3 - progestogen only implant, progestogen-only injectable
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Teratogenic risk Women (inc. their partners) who are taking teratogenic drugs (e.g. lithium or sodium valproate): Highly effective contraception is recommended - such as LARC If wishes to use COCP or POP - should use additional contraceptives (such as condoms)
Liver enzyme inducers and drug interactions Inducers Inducers can interact with, and reduce the efficacy of hormonal contraception Offer LARCs which are unaffected (CU-IUD, LNG-IUS, Depo injection) Inducers include (PCBRAS) Phenytoin Carbamazepine Barbiturates Rifampicin Alcohol (chronic xs) and Antiretrovirals (-avirs and NNRTIs) Sulphonylureas, St John’s Wort Drug interactions Note - Lamotrigine is NOT an inducer BUT may interact with POP/CHC - avoid CHC (reduces lamotrigine efficacy - inc. seizure risk), POP inc. lamotrigine levels increasing adverse effects etc.
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Oral contraceptives - Missed Pill Rules Progestogen-Only pill
A missed pill is defined as any pill > 3 hours late (if missed by < 3hrs, take as normal) Exceptions - desogestrel POP = 12 hours, Drospirenone POP = 24 hours Advice: Take missed pill now Use additional precautions for the next 48 hours Emergency contraception is needed if they have had sex since missing the pill OR within 48 hours of restarting the regular pills Nb. Irregular periods are the most common side effect of POP
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Combined oral contraceptive pill Missed pill is defined as any pill which is > 24 hours late Advice 1 missed pill - take the missed pill now, as soon as it is remembered (even if 2 taken on the same day), and then continue as normal. No extra precautions needed. 2 missed pills Take a pill now (as soon as remember), (even if 2 on the same day) Extra precautions needed for 7 days AND: If missed pill from 1st 7 in packet - need emergency contraception If missed pill from last 7 in packet - start the next packet without the pill-free week
Vomiting and diarrhoea Vomit within 3 hours - take another pill V&D for > 24hrs Follow missed pill rules (counting each day of V&D as 1 missed pill) Avoid sex or use barrier during illness and 7 days after
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Investigating dysmenorrhoea It is necessary to exclude underlying pelvic pathology before making a diagnosis of primary dysmenorrhoea. Investigations include: Pelvic US - to identify fibroids, endometriosis High vaginal/endocervical swabs - R/O STI Pregnancy test
Dysmenorrhoea Background Dysmenorrhoea - menstruation related abdominal pain Primary dysmenorrhoea Dysmenorrhoea in the absence of underlying pelvic pathology, usually in young women Suggested by History of dysmenorrhoea beginning approx. 6 months after commencing menarche Cramping lower abdominal pain which starts just before menstruation and lasts for 2-3 days Secondary dysmenorrhoea Dysmenorrhoea secondary to underlying pelvic pathology. Causes include: endometriosis, adenomyosis, pelvic inflammatory disease, fibroids Suggested by: Painful periods - which were previously not painful, or different pain Irregular pain history - often starting 3 or 4 days before menstruation, or continuing after. Other gynaecological symptoms are present - vaginal discharge/bleeding, dyspareunia, menorrhagia
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Management of Primary Dysmenorrhoea
Step 1 1st Line: NSAID (ibuprofen, naproxen, mefenamic acid) Add paracetamol if required, or prescribe PCM alone if NSAID not tolerated/CI Alternative - If does not want to conceive - trial a hormonal contraceptive for 3-6 months(e.g. COCP) Step 2 Combination of NSAID (or paracetamol) + COCP The management of secondary dysmenorrhoea depends on the cause (see other notes on endometriosis/fibroids/PID)
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Endometriosis Pathophysiology The presence of endometrium-like tissue outside of the uterine cavity (commonly within pelvis), which undergoes bleeding, inflammation and scar tissue formation in response to the hormonal changes of the menstrual cycle.
Clinical features Secondary dysmenorrhoea Chronic pelvic pain Deep dyspareunia Sub/infertility Bowel symptoms - e.g. pain on defecation Investigations Diagnosis - can only be confirmed by laparoscopic visualisation of the pelvis (findings include blood filled, ‘chocolate cysts’ - endometriomas) Other invx: TVUS, TAUS Management Refer for specialist assessment Endometriosis pain management Consider a trial of paracetamol and/or NSAID Offer hormonal treatment - COCP or POP, implant, mirena, depot Secondary care management includes surgery
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Adenomyosis
Adenomyosis Pathophysiology Extension of endometrial tissue into the uterine myometrium Clinical features Menorrhagia Irregular periods Dysmenorrhoea Diagnosis MRI imaging - an enlarged uterus, with thickened myometrium
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Ectopic Pregnancy Implantation of a fertilised ovum outside of the uterine cavity. Most commonly within the fallopian tube. Clinical features Symptoms - usually occur 6-8 weeks after the last menstrual period Abdominal pain PV bleeding Syncope/dizziness Amenorrhoea Examination findings Abdominal tenderness +/- peritonism (guarding, rebound tenderness) Pelvic tenderness Cervical motion tenderness Abdominal distension Haemodynamic compromise - suggests a ruptured ectopic pregnancy and intra-abdominal bleeding - tachycardia, hypotension, shock, orthostatic drop, pain in tip of shoulder (due to diaphragmatic irritation)
Investigations Transvaginal ultrasound is the diagnostic investigation of choice for EP. Beta-HCG levels should be obtained to guide management. Management Management options include watchful waiting, medical mx or surgical intervention Expectant management Uncommon, but an option if clinically stable and pain free, and hcg < 1500 Medical management Criteria: No significant pain, unruptured and no h/d compromise Serum hcg is < 1500 and adnexal mass is < 35mm Able to return for follow up 1st line: Methotrexate Nb. Patient must wait 3 months before trying to conceive again due to teratogenic effects
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Ectopic pregnancy
Surgical management Salpingectomy or salpingotomy - laparoscopic approach preferred Indications: Not able to return for follow up Significant pain Adnexal mass > 35mm Foetal heartbeat is present Serum hCG > 5000 Options: If the contralateral tube is healthy - salpingectomy should be performed If there is a history of factors associated with reduced fertility (prev. Ectopic, PID, abdo surgery, tubal damage) - salpingotomy should be considered All rhesus negative women who undergo surgical management require anti-D immunoglobulin If the hcg is 1500-5000, a choice between medical or surgical management can be offered, as long as the mass is < 35mm, and no significant pain/h/d instability.
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Endometrial cancer
Endometrial Cancer Background A common, oestrogen-dependent malignancy, which is preceded by endometrial hyperplasia, which subsequently progresses to malignancy. Any post-menopausal bleeding should be considered endometrial ca. until proven otherwise. Clinical features - Red flags & Referrals Post-menopausal bleeding is defined by NICE as unexplained PV bleeding > 12 months after menstrual cessation due to the menopause. Post-menopausal bleeding in women > 55 years- Refer as 2 week wait (via suspected cancer pathway) If < 55 years “consider a 2WW referral as above” Consider a direct access US scan for the assessment of endometrial cancer in any woman who is aged 55 or over with: Unexplained vaginal discharge and. 1st presentation of this OR thrombocytosis OR report haematuria Visible haematuria and.. Anaemic OR thrombocytosis OR hyperglycaemic
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Emergency Contraception Emergency contraception can be used following UPSI to prevent unintended pregnancy. There are 3 methods of emergency contraception. The copper IUD Oral ulipristal acetate Oral levonorgestrel Methods of Emergency Contraception The copper intrauterine device The most effective (pregnancy rate < 0.1%) Mechanism of action: Toxic to sperm and ova, prevents fertilisation If fertilisation does occur, the CU-IUD induces inflammation of the endometrium preventing implantation Timing: Within 120 hours/ 5 days of UPSI Adverse effects/Complications: Perforation of the uterus - 0.2% risk Expulsion - 5% risk Pelvic inflammatory disease Ectopic pregnancy - risk is very low due to effective contraception (but if pregnancy were to occur, there is a greater chance that it would be ectopic). Bleeding - frequent, irregular, prolonged bleeding for first 6 months can occur Contraindications (UKMEC 4): Post-abortion, postpartum sepsis Unexplained vaginal bleeding Cervical cancer Endometrial cancer Current symptomatic chlamydia, gonorrhoea or pelvic TB Current pelvic inflammatory disease
Oral ulipristal acetate - 30mg once only (ellaOne) Mechanism of action: Progesterone receptor modulator Suppresses the LH surge responsible for ovulation, therefore inhibiting/delaying ovulation Timing: Within 120 hours/ 5 days UPSI Not suitable if: using liver enzyme-inducing drugs (PCBRASS) Oral levonorgestrel (progestogen) - 1.5mg once only Mechanism of action: Prevents/delays follicular rupture, disrupting luteal function, and inhibiting ovulation Timing: Within 72 hours/ 3 days UPSI Note - can be used up to 96 hrs but efficacy decreases with time, so UA is preferred If on enzyme inducer, offer Cu-IUD as LNG effectiveness can be reduced. If Cu-IUD is not appropriate, a double dose of LNG (3mg) can be considered but women should be informed that the effectiveness of this regimen is unknown. Oral EC and Vomiting Both UA and Levonorgestrel can cause vomiting If a woman vomits within 3 hours of taking UA/levonorgestrel, a repeated dose is required Choosing which method of EC 1st line: Copper-IUD The most effective Offer to all women 2nd line: If criteria for insertion of Cu-IUD are not met, it is contraindicated (e.g. PID/STI etc) or if the woman does not want the Cu-IUD, offer oral EC. If > 72 hours - choose ulipristal acetate (ellaOne) - can be used up to 120 hours If on a liver-inducing drug (PCBRAS) Avoid ulipristal acetate Consider levonorgestrel double dose (if Cu_IUD cannot be offered) References FSRH Guideline: Emergency contraception [March 2017, amended July 2023]. Available at URL: https://www.fsrh.org/Common/Up...
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