O&G

1.most common places for ectopic pregnancy

2. risk factors

3. assessment/investigations ( assuming haemodynamically stable)

1. Tubal - ampulla of fillopian tube 70% , isthmus 12%, non tubal rare

2. Tubal damage / altered motility

prev ectopic, PID, pelvic surg, maternal age >35, smoking, endometriosis, IUD

3.

-physical exam,

- hx,

-transvaginal US - BHCG 1500-3000 gestational sac should be present , if empty uterus ectopic until proven otherwise

- beta HCg every 48hrs - >53% rise is normal ( slow or fall indicates ectopic)

1.clinical features of ectopic pregnancy

2. treatment

1. lower abdominal guarding/ pain ( similar presentation to appendicitis) colicky -> constant, +-PV bleeding, symptoms of pregnancy, shoulder tip pain, hypotension, taccy, presyncope, rebound tenderness -suggest rupture

2.

- expectant managment - requires b-hcg until 0

Medical management

- methotrexate ( not on live ectopic) bHCG <5000

- SE's avoid alcohol and folate, abdopain, photosensitivity

surgical management

- salpingectomy ( surgical laparoscopy) indicated in haemodynamically instabilty/ ruptured

ovarian torsion

1.definition of ovarian torsion

2.epidemiology

3.risk factors

1. twisting of the ovary around adnexal ligaments

2. child bearing age women

3. ovary enlargement : cysts, tumours,PID, pregnancy, laxity of pelvic/suspensory ligament, strenuos exercise

ovarian torsion

1. presentation

2. assessment

3. mangement of ovarian torsion

1. sudden onset unilateral lower abdominal pain( can fluctuate - intermittent torsion), nausea vomiting, +- palpable adnexal mass

2. ultrasound :

- symmetrical ovariaes of normal volume, torsion unlikely

- absence of doppler flow is late sign of torsion

3. emergency exploratory laparoscopy - adnexal detorsion

aetiology and high risk age group for PID

upper gential tract infection which can cause endometriosis, perotinitis, salpingitis, tubo-ovary abcess

pathogens : chlamydia trachomitis , gonorrhea neisseria

high risk age group - 16-24

epidemiology - 18-44

PID

1. risk factors

2. assessment

3. treatment

4. complications

1. multiple sexual partners, STIs, vaginal douching, unprotected sex, IUDs

2. bimanual exam - cervical motion tenderness minimum criteria ( low threshold for diagnosis), adnexal tenderness

clinical diagnosis

3. remove infection - empiric antibiotics ( start if PID suspected), STI screen,

counselling, follow up, partner screening, no intercourse

4. infertility , chronic pelvic pain , ectopic pregnancy

cord blood tests at delivery

cord blood tests at delivery:

fetal blood group ( check for rhesus D +)

antibodies attached to fetal red cells - coombs test

fbc

bili rubin - only if severe

complications of VBAC

complications of VBAC

1. uterine scar rupture influence by type of cesarian ( high uterine, inverted T or low vertical uterine) and labour inducing medications

2. chance of needing assisted birth - forceps

3. chance of emergency c section

4. risk of injury to perineum and/or pelvic floor

suitabiltity for VBAC

factors supporting and against

supportive factors

- previous vaginal birth

- c section was due to breech or non head down postion

- c section was not from prolonged labour due to maternal hypertension or preterm birth

factors resulting in higher likely hood of emergency C section

- labour augementation ( meds to help speed up labour)

- BMI >40 at start of pregnancy

- gestational diabetes

- age >35

- baby size > average gestational age

pros and cons VBAC vs planned caesarean

don’t forget general surgical complications

5 common genetic screenings and purpose for screening

1.CF

2. spinal muscular atrophy

3. fragile x

4. thalassemia

5. sickle cell

6. duchenne/becker muscular dystrophy

tests persons DNA to pathogenic variants, identifies reproductive risk, allows informed choices ( IVF, preparation, termination), reduce risk and mortality from congenital born disease

what are the principles of Autosomal recessive genetic inheritance

both parents carriers = 25% affected, 50% carriers, 25% unaffected

e.g CF, SMA, thallesemia

prenatal testing for both parents

what are the principles of Autosomal dominant genetic inheritance

one affected parent = 50% chance of affected child

e.g marfans, huntingtons

what are the principles of x linked recessive recessive genetic inheritance

* affects sons more ( male to male transmission cannot occur)

- carrier mother = 50% affected sons, 50% carrier daughters

- carrier father = carrier daughters, no affected sons

e.g duchenne, haemophilia A

what are the principles of x linked dominant genetic inheritance

- Affected mothers → 50% affected children

- Affected fathers → all daughters affected, no sons affected

Examples: Fragile X syndrome

Card 1 — Physiology of Labour

Q:What hormonal and mechanical factors initiate and maintain labour?Include roles of oxytocin, prostaglandins, Ferguson reflex, and myometrial gap junctions.

A:

Prostaglandins (PGE2, PGF2α) soften and ripen the cervix + increase uterine contractility.

Oxytocin from the posterior pituitary increases contraction strength; also stimulates prostaglandin release.

Ferguson reflex: fetal head stretches cervix → ↑ oxytocin → ↑ contractions (positive feedback).

Myometrial gap junctions increase → coordinated contractions across uterus.

Stages of Labour

Q:What are the three stages of labour, and what defines the latent vs active phase of Stage 1?

A:

Stage 1: Onset of contractions → full dilation.

Latent: ≤4 cm dilation, painful contractions.

Active: ≥5 cm dilation, painful regular contractions, rapid cervical change.

Stage 2: Full dilation( 10cm) → delivery of baby (passive + active/pushing phases).

Stage 3: Delivery of baby → expulsion of placenta (physiological or active management).

Stage 4: monitor for PPH or preeclampsia

Q:What are the key management steps during the first stage of labour?

A:

- Offer analgesia on request.

- CTG (intermittent or continuous).

abdo exam

- Assess fetal position/lie ( if unclear use ultrasound)

• how many 5ths palpabable is the head ( 2/5ths means engaged with pelvis)

• ask about fetal movements

- vaginal exam

BISHOP

• cervix effacement

• station of baby ( 0 = at level of ishial spines)

• hardness/soft consistency of cervix?

• opening- how dilated

• position of uterus - retro(-1 point) or anterverted

Q:What are the key management steps during the second stage of labour?

A:

Assist the mother to find comfortable, safe positions for pushing.

Guide fetal delivery through the vaginal canal (support cardinal movements).

Delay cord clamping for at least 30–60 seconds.

Q:What are the key steps in active management of the third stage of labour ( delivery of placenta)

A:

Active management reduces risk of postpartum haemorrhage.

Give oxytocin → increases uterine tone, reduces blood loss.

Perform controlled cord traction (Brandt–Andrews manoeuvre) if placenta not delivered spontaneously.

Inspect placenta for complete cotyledons, intact membranes, and three cord vessels (1 vein, 2 arteries).

Repair any obstetric lacerations.

Normal Labour Progress

Q:What characterises normal progress in the first and second stages of labour?

A:

First stage: Steady cervical dilation from 5 cm onward; contractions become stronger/closer; progressive fetal descent.

Second stage: Descent + rotation → effective pushing; delivery within ~2 hr nulliparous, ~1 hr multiparous (longer acceptable if maternal/fetal status reassuring).

Abnormal Labour Progress

Q:What defines slow/arrested labour in Stage 1 and Stage 2?What are common causes?

A:

Stage 1 slow labour: <2 cm dilation over 4 hr after reaching ≥5 cm.

Stage 2 arrest: No descent despite adequate contractions/pushing.

Causes (3 Ps):

Power: inadequate contractions

Passenger: malposition (OP, asynclitism), macrosomia

Passage: cephalopelvic disproportion (CPD)

list pharm and non pharm pain relief options during labour

risks of opioids and epidural

A: non pharm

Support / continuous labour companion → reduced fear; improved coping.

Water immersion → buoyancy, relaxation.

TENS → gating pain pathways.

Hypnobirthing, breathing, relaxation → reduces sympathetic tone.

Heat packs, massage, position changes → reduce muscle tension and improve comfort.

A: pharm

Nitrous oxide: quick, self-administered; mild analgesia.

Opioids (morphine, fentanyl): moderate analgesia; cross placenta → neonatal resp depression.

Epidural: most effective; risks: hypotension, prolonged second stage, instrumental birth.

Pudendal block / local infiltration: used in second stage or for instrumental birth.

4 components of CTG and etiology of FHR alterations

Baseline rate,

- 110 -160 bpm

Variability

- reduced or absent = concerning

Accelerations

- >2 accerlations over 20 mins = reactive FHR tracing

Decelerations.

- a temporary decline in the FHR of > 15 bpm for a maximum duration of 3 minutes

VEAL CHOP

Variable decelerations→ Cord compression/prolapse

Early decelerations→ Head compression

Accelerations→ OK

Late decelerations→ Placental insufficiency/Problem

Maternal Indications for Unplanned Caesarean

Q:List maternal reasons for unplanned intrapartum caesarean.

A:

-Failure to progress (Stage 1 arrest or Stage 2 arrest).

-Obstructed labour (CPD, shoulder dystocia ).

-Maternal exhaustion inhibiting progress.

-Severe maternal illness (eclampsia, haemorrhage, sepsis).

Fetal/Placental Indications

Q:List fetal and placental indications for unplanned caesarean delivery.

A:

-Abnormal CTG / non-reassuring fetal status.

-Failed instrumental delivery.

-Malpresentation (transverse, brow, unstable lie).

-Cord prolapse.

-Significant placental abruption.

-Vasa praevia with bleeding.

fetal and maternal life threatening complications of delivery

Life-threatening complications

-Prolonged second stage of labor

- Obstructed labor, e.g., due to shoulder dystocia

- Umbilical cord complications,

including nuchal umbilical cord

- Uterine rupture

- Uterine inversion

- Postpartum hemorrhage

- Amniotic fluid embolism

perineal tear laceration classification

1 - cutaneous to subcutaenous - no involvement of perineal muscles

2 - 1st degree plus laceration to perineal muscles

3 - 2nd degree plus involvement of external (+- internal) sphincter ( may lead to faecal incontinence)

4 - 3rd degree plus laceration to anal mucosa

Treatment for perineal lacerations 1& 2nd stage vs 3rd & 4th

complications of 3rd & 4th stage repairs

1st & 2nd

Conservative - nsaids & sitz baths

suture - local anesthesia - continous sutures or surgical glue

3rd & 4th

regional or GA used

reconstructive surgery

Complications Primarily associated with third- and fourth-degree lacerations.

- Pain and dyspareunia

-Rectovaginal fistulae

-Hemorrhage

- Infection

-Wound dehiscence

Prevention: application of warm compress to perineum during delivery

epidemiology and risk factors for perineal tears

Epidemiology: most common obstetric injury of the pelvic floor

Risk factors

-Macrosomia

- midline episiotomy

-Forceps delivery

-No previous delivery

-Prolonged second stage of labor

-Occiput posterior delivery

-Rapid delivery of head in breech presentation

-Head extension before crowning

-Lack of perineal elasticity (e.g., perineal edema)

define gestational hypertension vs preeclampsia vs eclampsia

Gestational hypertension = new BP ≥140/90 mmHg after 20 weeks with no proteinuria or end-organ dysfunction.

Pre-eclampsia = new hypertension plus either proteinuria, or maternal organ dysfunction, or foetal growth restriction/placental dysfunction

Eclampsia = generalised tonic-clonic seizures in a woman with pre-eclampsia, not explained by another neurological cause.

* chronic hypertension = hypertension during pregnancy present <20 weeks

List major maternal complications of pre-eclampsia.

Eclampsia, HELLP syndrome, AKI, pulmonary oedema, DIC, placental abruption, stroke/cerebral haemorrhage, ICU admission, increased long-term CV risk.

what is HELLP syndrome

What is the cure?

what siezure prophylaxis is given in this condition along with eclampsia?

Preeclampsia with thrombotic microangiopathy involving the liver

HELLP = Hemolysis, Elevated Liver Enzymes, and Low Platelets

(clots in liver causing liver dysfunction -> liver failure, DIC)

cure = delivery of placenta

IV magnesium sulphate 4mg infusion over 20 mins

List major fetal complications of hypertensive disorders of pregnancy.

Fetal growth restriction

Preterm birth

Seizure-induced fetal hypoxia

Fetal death

oligohydramnios ( amniotic fluid lower than normal = poor nourishment - premature birth)

Q:What investigations are required for a pregnant patient with new hypertension?

BP measurement:

Urinalysis: urine protein:creatinine ratio (uPCR) or 24-hr protein if required

- uPCR ≥30 mg/mmol = proteinuria

Bloods: FBC (platelet count), renal function (creatinine, electrolytes), LFTs

Foetal assessment: CTG if concerns,

Baseline observations: fluid balance, oxygenation, neurological status.

Q:What antihypertensive agents are used in pregnancy, and when do you urgently treat?

A:Urgently treat BP ≥160/110 mmHg.

First-line agents:

Hypertensive Moms Need Love

hydralazine (IV) - urgent

Methyldopa for chronic BP control ( oral)

nifedipine (oral IR),

labetalol (IV/oral) - urgent

prophylaxis for high risk pre eclampsia

aspirin 100-150mg daily ( racgp guidelines)

initiated between 12-28 weeks gestation

delivery plan/timing in hypertensive Pregnancy disorders

- immediate stabilisation for patient with preeclampsia with severe featuers, eclampsia or HELLP

-assess gestational age:

Severe pre-eclampsia ≥34 wks → deliver after stabilisation.

Severe pre-eclampsia <34 wks → intensive monitoring; deliver if maternal/fetal deterioration.

Mild pre-eclampsia ≥37 wks → deliver.

Gestational hypertension → expectant management until term unless it progresses.

Q:What are the key steps in the acute management of eclampsia?

ABCs + left lateral position + oxygen

Magnesium sulfate (4 g IV loading, then 1 g/h infusion; repeat 2 g if seizure recurs)

Control severe BP ≥160/110 with labetalol/nifedipine/hydralazine

- Monitor for mag toxicity

- reflexes, respiratory rate, urine output; have calcium gluconate ready

-Blood tests (FBC, LFTs, renal function, coagulation)

- Plan delivery once stabilised (definitive treatment)

pathophys of preeclampsia

abnormal placental invasion/ development -> hypoperfused placenta releases inflammatory cytokines and anti angiogenic factors systemically

-Capillary leak (→ oedema, pulmonary oedema)

-Vasoconstriction (→ hypertension)

-Platelet activation & microangiopathy (→ HELLP, organ dysfunction)

-Cerebral endothelial dysfunction → impaired cerebral autoregulation , disruption of BBB- cerebral oedema- eclampsia

Q: What is the definition of primary and secondary postpartum haemorrhage?

A:

Primary PPH:

≥500 mL blood loss in first 24 hrs postpartum

≥ 100mls after c-section

or any blood loss causing haemodynamic instability.

Secondary PPH: Abnormal bleeding from 24 hrs to 6 weeks postpartum

Q: What are the 4 Ts causes of PPH, and what do they represent?

A:

Tone: Uterine atony - cant contract/compress vessels (most common ). prolonged labour, mag sulfate, overdistended uterus, infection 70-80%

Tissue: Retained placenta, membranes, cotyledons, clots. 10%

Trauma: Genital tract tears, episiotomy, uterine rupture. 10-20%

Thrombin: Coagulopathy (DIC, pre-eclampsia, HELLP). 1-4 %

Q: What are key strategies for PPH prevention and early recognition?

A:

Prevention: Active management of third stage — oxytocin, controlled cord traction, uterine massage.

Recognition: Quantify blood loss, monitor vitals, assess uterine tone, inspect genital tract, recognise boggy uterus or persistent bleeding.

Q: What is the stepwise management of PPH?

A:

1.Call for help, ABCDE, 2x large-bore IV access, fluids ( warmed crystalloid), bloods ( FBC, coags, fibrinogen, group and hold).

2.Identify 4 Ts, empty bladder, uterine massage.

3.Uterotonics: oxytocin → ergometrine ( not in hypertension) → carboprost (not in asthma)→ misoprostol.

4. Tranexamic acid (1 g IV) within first 3 hours, repeat after 30mins if still bleeding .

5. Mechanical measures: bimanual compression, balloon tamponade.

6. Surgical/IR: EUA + repair tears, manual removal, curettage, uterine artery ligation, B-Lynch sutures, uterine artery embolisation, hysterectomy.

Q: What are the indications for surgical intervention in PPH?

A:

Failure of uterotonics + mechanical methods + TXA.

Retained placenta/products needing removal.

Genital tract trauma requiring repair.

Suspected placenta accreta spectrum or uterine rupture.

Life-threatening haemorrhage → peripartum hysterectomy if conservative measures fail.

Q: What are the indications for blood transfusion in PPH

A:

Ongoing significant bleeding or haemodynamic instability.

Hb <70 g/L (or higher threshold if symptomatic).

FFP: INR >1.5 or massive haemorrhage.

Platelets: <50 ×10⁹/L with bleeding.

Cryoprecipitate: Fibrinogen <2 g/L or DIC

Massive transfusion protocol if large/rapid blood loss.

- plus calcium

ratio 1 RBC: 1 FFP : 1 platelets

Q: What is shoulder dystocia?

An obstetric emergency in which the anterior shoulder of the fetus becomes impacted behind the maternal pubic symphysis during vaginal delivery, or, less commonly, the posterior shoulder becomes impacted against the sacral promontory

risk factors and a clinical sign for shoulder dystocia

1.History of shoulder dystocia

2 anything that could make baby big:

-Fetal macrosomia, Maternal diabetes mellitus or gestational diabetes, Maternal obesity

3. Prolonged second stage of labor

*many cases occur in absence of risk factors

clinical sign

- turtle sign - retraction of partially delivered head against perineum

fetal and maternal complications of shoulder dystocia

Maternal: PPH, 3rd/4th degree tears, symphyseal injury, uterine rupture (rare).

Fetal: Brachial plexus injury (Erb palsy C5-6 brachial plexus), clavicle/humerus fracture, hypoxia, HIE hypoxic ischemic ecephalopathy, death.

management of shoulder dystocia

first line

internal

last resort

FIRST LINE

McRoberts manoeuvre (hips hyperflexed - flattens sacrum)— resolves ~40–50%.

+

Suprapubic pressure (downward/lateral to disimpact shoulder)

.Never apply fundal pressure.

INTERNAL

Rubin II: Pressure behind anterior shoulder → rotate.

Woods Screw: Pressure on posterior shoulder → rotate like a corkscrew.

Gaskin : mother on all fours

LAST RESORT

Cleidotomy (fracture clavicle),

Zavanelli manoeuvre (flex head → replace → emergency CS),

definition of still born vs death of a neonate. where do you legally report?

still born = no signs of life at ≥20 weeks of ≥400g birthweight ( if gestation unknown)

neonate death:

between 0-28 days

0-7 early, 8-28 late

report a still born or neonatal >20 weeks or 400g death with registry of births deaths and marriages

- provide stillborn certificate

causes of stillbirth

1. congenital anomolies

- structural (anencepaly, tet of fallot, gastrochesis, or chromosonal )

2. placental pathology

- ruptured, insufficiency, infarction, cord accident

3. maternal conditions

- HTN, diabetes, uterine rupture, Fetal maternal haemmorage ( alloimunisation), heavy smoking

4. feotal conditions

- hypoxia, FGR, alloimmunisation

5. infection

congenital, MUM , bub , placenta , infection

investigations after stillborn and management

1. hx ( find out risk factors or symptoms)

2. maternal ix

- fbc, blood group , antibodies

- Hba1c

- thyroid

- thrombophilia

3. placental exam

- Cord insertion, knots, thrombosis, infection, infarction.

- macroscopic and histopath

4. baby exam

- autopsy or xray .

how to determine feotal growth restriction ( FGR)

risk factors

estimated feotal weight or abdo circumference is <10% for gestational age.

maternal: smoking, hypertension , autoimmune

placental: abnormal implantation, infarct

fetal: aneuploidy/chromosomal, infections ( Toxoplasmosis, syphilus, CMV, malaria)

TORCH infections are vertically transmitted and can cause feotal pathology and death. what does the mnemonic stand for

Toxoplasmosis - cats host- chorioretinitis, diffuse brain calcificaitons

Other ( syphilius, listeria, HIV, varicella)

Rubella

Cytomegalovirus ( CMV) - herpes latent infection , sensoneural hearing loss and periventricular brain calcifications

Herpes simplex virus (HSV)

management of stillborn

spontaneous labour often occurs within 2 weeks of intrauterine death

misopristol or oxytocin IV infusion

Define PROM and PPROM.

clinical presentation and management of chorioamniotnitis

PROM: Prelabour rupture of membranes at ≥37 weeks before labour begins.

PPROM: Preterm Prelabour rupture of membranes <37 weeks.

- fever, uterine tenderness, maternal and fetal tachycardia

- broadspectrum antibiotics + delivery

Q: What are the key maternal and fetal risks associated with PROM/PPROM?

A:

Maternal: Chorioamnionitis, sepsis, endometritis, placental abruption.

Fetal: Infection, cord prolapse/compression, prematurity (in PPROM), pulmonary hypoplasia (early PPROM), perinatal morbidity/mortality.

Outline the key management strategies for PROM and PPROM.

A:

PROM (≥37 weeks):

- speculum, check for pooling of fluid, signs of choriamnionitis, assess maternal vitals and fetal wellbeing

- deliver / expectant or IOL within 24hrs

- check if GBS postive - intrapartum antibiotics

PPROM (<37 weeks):buy time .

deliver if infection, fetal compromise, or at appropriate gestation.

1. corticosteroids - bethamethasone 12mg IM ( given up to 36 +6 weeks)

2. tocolytics - nifidepine - stop contractions

3. mag sulfate if <32 weeks

4. antibiotics - amoxycillian 2g IV + azythromycin 1g PO once

Antenatal corticosteroids: indications, mechanism, and dosing

Purpose: Accelerate fetal lung maturation in threatened preterm birth

Benefits:

-↓ Neonatal respiratory distress syndrome (RDS)

- reduce risk of Intraventricular haemorrhage (IVH)

- reduce risk of Necrotising enterocolitis (NEC)

Mechanism: Stimulates type II pneumocytes → ↑ surfactant production.

Dosing:

Betamethasone: 11.4 mg IM × 2 doses, 24 h apart

Dexamethasone: 6 mg IM × 4 doses, 12 h apart

Indications: preterm labour, planned early delivery -pre-eclampsia

frequency of contractions in active labour

stage 1 - every 10 mins

stage 2

- early - every 4-10mins

- late - every 2 mins

what are braxton hicks

benign contractions helping with the position of fetus

- often occuring in 2nd/3rd trimester

- duration for <1min

epidemiology and risk factors for breast cancer

occurs in 1:7 women

92% survival >5 years

RF

1. increased estrogen exposure 85% of all cancers

- nulliparity

- late first pregnancy

- early menarche/ late menopause

- HRT

- OCP

2. Genetic

- BRCA 1/2 . P53 mutations

- first degree relative breast Ca hx

- previous breast CA

3. Other

- alohol

- obestiy

- dense breast tissue

- previous radiation hx

Screening is available for which age group and what is its purpose.

50 -74 mammogram ( every 2 years)

- can start by age 40 upon request

purpose is to reduce development to palpable mass

What is the most common breast cancer and how it spreads

Invasive Ductal Carcinoma

lymphatic:

axillary lymph nodes, internal mammery, supraclavicular

haematogenous

- bone - most common symptomatic site

- lung

- live

-brain

* lobular carcinoma- more diffuse - GI and peritoneoum, ovary involvemnt

Management for breast cancer

Triple Assessment

1. hx & clinical exam

2. Imaging

< 35 - US

> 35 mammogram -+ US

3. core biopsy ( diagnostic)

triple test is positive if any of 3 components supicious

* use MRI in dense breasts

Staging - TNM

CT abdo chest pelvis if symptoms or node positive

PET - CT in higher stages

Key molecular drivers in breast cancer and their cancer treatment

why does triple neg have the worst prognosis

estrogen receptor - estrogen inhbitor - Tamoxifen or aromatase inhibitor ( post menopausal)

progesterone receptor

Human Epidermal growth FActor HER2 - Trastuzumab/ herceptin

^^ easy drug targets

when breast cancer is negative ER, PR , HER2 the only treatment option is chemo

risk difference between BRCA1 vs 2 mutation

BRCA1 - triple neg tendancy + ovarian

Lifetime breast cancer risk: 60–85%

Lifetime ovarian cancer risk: 40–60%

Cancers tend to be triple-negative and high-grade

Earlier onset

Also increases prostate cancer risk in males

Exam trick: BRCA1 → “1 letter away from TN” → Triple Negative tendency

BRCA2 - lower risk for breast higher for other

Lifetime breast cancer risk: 50–85%

Ovarian cancer risk: 10–30%

Cancers more often ER-positive

Also increases pancreatic and prostate cancer

prognosis and treatment for luminal a, B HER2 , triple neg

luminal a - BEST - endocrine therapy

luminal b - MODERATE - endocrine + -chemo

her 2 positive - GOOD with treatment - anti her 2 + chemo

triple neg - WORST - chemo +- immunotherapy

clinical features , investigations, management of inflammatory breast cancer

rapid-onset red ≥ 1/3rd of breast

swollen breast with peau d'orange from dermal lymphatic invasion;

no response to antibiotics within 7-10 days

high metastatic potention

investigations

punch biopsy

mammogram/ultrasound (<30)

Management:

requires neoadjuvant chemo → mastectomy → radiation.

* often misdiagnosed as mastitis

sensation to the external genitalia/perineum is provided by which nerve

pudendal

First trimester - key physiology + risks

0-13 weeks

Organogenesis (5-10 weeks) → highest teratogen risk

hCG maintains corpus luteum → progesterone support

Spiral artery remodelling begins

Main risks: miscarriage, ectopic, hyperemesis

First trimester - essential tests & why

1.Dating scan ( US crown - rump length) → most accurate GA within 5-7 days. done at weeks 7-10

2. FBC, group & antibodies → anaemia + HDFN( haemolytic disease of fetus & newborn) risk

3. Infectious screen (HIV, Hep B/C, syphilis, rubella) → prevent vertical transmission

4.MSU → asymptomatic bacteriuria - increased risk of pyelonephritis and preterm delivery

5. NT ± NIPT (10-13 w) → aneuploidy screening

NIPT vs NT, when best done

NT - nuchal translucency providing first physical anatomy check of baby - US measuring neck fluid for chromosomal and structural/cardiac abnormalities

10-16 weeks best done

NIPT - most accurate genetic screening for Downs

syndrome - measure free fetal maternal DNA

12 /13 weeks

Second trimester - key physiology + complications

Weeks 14-27

Placenta fully functional

Rapid fetal growth

hPL (human placental lactogen)→ ↑ insulin resistance

Plasma volume expansion peaks

compilcations:

Gestational diabetes

Cervical insufficiency- uncommon cause of SAb

Placenta previa

Preterm labour (viability ~23-24 weeks in Aus)

Second trimester - major screening

18-22 w morphology scan → structural anomalies + placenta location

24-28 w OGTT → gestational diabetes - prevent neonatal hypoglycemia

Maternal quad screen ( if no prev NIPT) - AFP, hCG, estriol, inhibin A

Fundal height (from 24 w) → growth screening

Amniocentesis (if indicated) → diagnostic genetics

Third trimester - physiology + surveillance focus + major complications

how to determine between placental abruption vs previa

Weeks 28-40

Rapid fetal weight gain

Hypercoagulable state

surveillance focus:

BP + urine each visit → preeclampsia screen

Monitor movements + presentation

complications:

Preeclampsia

FGR

PPROM

Placental abruption- cause of haemorrage - painful , rigid uterus

placenta previa - cause of haemorrage- painless ,soft uterus

Third trimester - key interventions

treatment for GBS positive mum?

28 w give Anti-D (if Rh-)

28 w FBC → anaemia

35-37 w GBS swab → intrapartum IV penicillin if positive

Growth scan if risk (GDM, HTN, FGR)

ECV( external cephalic version) at 36-37 w if breech

Rotterdam's criteria for PCOS

1. irregular/absent periods - oligo/anovulation

2. hyperandrogenism - clinical or biochemical

- clinical : acne, hirsutism

3. polyystic ovaries - ≥12 follicles on ultrasound

* need 2/3

pathophys of PCOS and what hormone levels you would expect to see in FSH + LH

PCOS = Fast GnRH → High LH → High Androgens → Follicles Arrest → no ovulation = No Progesterone from CL

increased androgens = increased visceral adiposity , impaired insulin signalling - pancreas compensates with increased insulin secretion

Insulin directly stimulates theca cells - increased androgen production

high LH and normal/low FSH

* high antimullarian hormone (AMH) - hinder maturation of follicles

treatment and complications of PCOS

OCP ( DIane 35) - regulates cycles, reduces free testosterone and endometrial hyperplasia

if wanting pregnancy - letrozole - aromatase inhibitor - decreases estrodial production = increased FSH = ovulation

BMI >25 - metformin - increase insulin sensitivity

hirsutism - spironolactone (androgen receptor blockade) - teratogenic - must give with contraception

first line always - exercise ( 5% weight loss can cause ovulation) , mediteranean diet

- gestational diabetes, T2DM

- infertility

- metabolic syndrome, dyslipedemia

- endometrial hyperplasia ( cancer) - unopposed estrogen

normal range for baseline fetal HR?

blood vessels in umbilical cord?

normal range for fetal hr variability?

1. 110-160

2. 2 arteries 1 vein

3. 5-25 bpm

depth of invasion

placenta accreta, increta, percreta?

accreta - chorionic villi adheres to myometrium

increata- chorionic villi invades myometrium

percreta - chorionic villi growth through myometrium

complications of PPH

Hypovolaemic shock

DIC

Renal failure

Sheehan syndrome - ischemic pituitary necrosis ( agalactorheaa earliest sign)

Maternal death

Risk factors for PPH

Antenatal :

Previous PPH

Multiple pregnancy

Polyhydramnios - chronic uterine distension - atony

Anaemia - poorer tolerance of blood loss

Fibroids- impaired uterine contractility

Intrapartum :

Prolonged labour

Induction/augmentation - myometrial fatigue - atony

Instrumental delivery

Caesarean section

Chorioamnionitis - reduced contractilty - atony

mifepristone vs misopristol

cut off for at home medical abortion?

surgical abortion preferred gestation dates

Mifepristone → progesterone antagonist ( stop pregnancy process) - egg detaches from uterine wall , uterus contracts

Misoprostol →synthetic prostaglandin - cervical ripening and uterine contractions -

9 weeks for at home ( later cut off at specialist hospitals)

14-22 weeks for surgical ( under GA or local)

complications of abortion

1. failure of abortion (1 in 100)

2. retained tissue ( 3-5 in 100 - medical)

3. infection <1-100

4. haemorrage - 1-1000

which ultrasound is used to detect fetal anemia?

what gestational age is this appropriate?

serial MCA - middle cerebral artery doppler - starting 16-18 weeks

- common in twin to twin transfusion syndrome, red cell alloimunisation

contraception options for breastfeeding women

progestrone only

- oestrogen can interfere with milk supply

what liver enzyme physiologically increases in pregnancy

name 3 liver dysfuncitons to be aware of in pregnancy

ALP

- presence of placenta ALP

ICP

intrahepatic cholestasis of pregnancy - increased oestrogen, impaired bile acid transport - maternal accumulation in blood - crosses placenta - risk of fetal arrythmia, still born.

itchy palms and soles

preeclampsia HELLP

- RUQ pain + thrombocytopenia in 3rd trimester → HELLP until proven otherwise.

AFLP

Acute fatty liver of pregnancy - fatty acid oxidation defect - fat depositions on liver - hypoglycemia cant produce ketones when fasting - liver failure - immediate delivery

( serum bile acid ≥10)

differentials for non pregnant/ abnormal uterine bleeding vaginal bleeding

PALM COEIN

structural

Polyp (endometrial polyp)

Adenomyosis

Leiomyoma (uterine leiomyoma)

Malignancy and hyperplasia

Nonstructural causes

Coagulopathy: e.g., Von Willebrand disease

Ovulatory dysfunction -anovulatory bleeding e.g., secondary to hyperprolactinemia, thyroid disorders, PCOS, obesity

Endometrial : endometrial dysfunction in a structurally normal uterus with regular cycles (diagnosis of exclusion)

Iatrogenic: e.g., estrogens, progestins, IUD, antithrombotic agents

Not otherwise classified : e.g., cesarean scar defect, uterine arteriovenous malformations (AVM)

adenomyosis vs leiomyoma

impact on uterus shape , pain, imaging, fertility

adenomyosis

- bulky uniformly enlarged uterus

- painful , heavy periods

- diffuse myometrial change

leiomyoma ( fibroid)

- focal mass/ irregular contour

- heavy periods but painless

- discrete mass

- submucosal impact on fertility

describe uterine hyperstimulation and management

excessive contractions of the uterus - ≥5 in 10 or a contraction >2mins

can be caused by induction agents - prostaglandins, syntocin

managent

remove inducing agents

position px to left lateral position ( improve blood flow)

give tocolytic

- IV or SC turbutaline 0.25mg

or nitroglycerine 60- 180 micrograms

when to give Anti D in pregnancy

and dosing for rhesus D prophylaxis

give at:

28 & 34 weeks

within 72 hours if baby RH+

any event with bleeding/procedure

< 12 weeks 250 IU

≥12 weeks 625 IU

don't give:

-if mother already sensitised

- baby confirmed negative

complications for preterm labour short

low birth weight

explain transient thyroid hyperemesis gravidarum

physiological response in pregnancy up to 12 weeks as HcG ( from corpus luteum) stimulates TSH receptors on thyroid causing increased free T4 - increased catecholimines sensitivity - activates vomiting centre, anxiety, tachy.

what RSV vaccine can be given to mother

mechanism of action?

benefits, side effects

abrysvo

given at 24-36 weeks to prevent RSV in infants

mechansim

targets pre-fusion F protein on RSV virus before it infects cell

must be given 2 weeks before birth for effectiveness protective for first 6 months

minimal side effects , no evidence on BW, prematurity, still births

50% less likely to be hospitalised with RSV during 6 months

* no maternal protection

* active immunity ( b&t cell activation) + passive immunity to fetus ( no memory cells)

Which RSV vax can be given to infants?

mechanism ?

when is it given?

benefit?

nirsevimab

a monoclonal antibody which binds to prefusion F protein inhibiting RSV from infecting cells

given at birth - if mother not effectively immunissed

given 7months-2 years at RSV season IF RISK FACTORS:

<32/40

congenital heart disease

immunosuppresion

chronic lung disease ( CF)

trisomy 21

* 80% risk reduction of hospitalisation in first year of life.

Types of Miscarriage

Q: What are the main types of miscarriage and how do they present?

🩸 Types

Threatened

Bleeding + cramping

Cervix closed

Viable pregnancy

Inevitable

Bleeding + cramping

Cervix open

No passage yet

Incomplete

Bleeding + cramping

Some products passed

Cervix open

Complete

All products passed

Cervix closed

Heavy Bleeding will settle

Missed

Fetal demise, no symptoms

Cervix closed

Often minimal bleeding

🧠 Exam memory line:

Closed = threatened/missed

Open = inevitable/incomplete

management of miscarriage

Unstable = surgery

Stable = expectant / medical / surgical

⚖️ Stable patients — 3 options

1. Expectant

Watch and wait

Suitable if mild symptoms

2. Medical

Misoprostol

Used for incomplete or missed miscarriage

* not necessary for mifepristone as pregnancy already nonviable

3. Surgical (definitive)

Suction curettage (vacuum aspiration)

Indications:

Heavy bleeding

Infection

Failed medical

⚠️ Always consider

Anti-D if Rh-negative

Infection → antibiotics

Follow-up to ensure complete evacuation