Olivia RANZCOG content Flashcards

Question

Poor predictors of tolerating pregnnacy with heart disease

Answer 1

1. Pulmonary hypertension ``` 2. High New York Heart Association class I - No breathlessness II - Breathlessness on severe exertion III - Mild exertion IV - At rest ``` 3. cyanosis (<80% oxygen saturations) 4. Haemodynamic compensation secondary to heart lesion

Answer 2

Systemic to pulmonary circulation (e.g. ASD or VSD) L --> R shunt increased pulmonary blood flow pulmonary vascular injury and increased pulmonary resistance R --> L shunting of blood with hypoxia and erythrocytosis

Answer 3

Increased right to left shunt in those with eisenmengers RHF Pulmonary hypertensive crises

Answer 4

Terminate (still 7% risk mortality) If continue pregnancy: sildenafil (vasodilator), elective admission for bed rest and oxygen, can have NVB, nothing that decreases afterload - avoid hypovoalemia, beta blockers, careful with regional anaesthesia and oxytocin

Answer 5

Blocks catecholamine action on beta receptors in heart and peripheral vasculature - Decreases BP - Decreases myocardial contractility and therefore oxygen demand on heart - Decreases CO - Decreases HR (slows conduction through AV node)

Answer 6

<1cm2 across valve. Normally caused by congenital bicuspid aortic valve. Manage less severe cases with beta blockers if LV not impaired.

Answer 7

Autosomal dominant

Answer 8

80% Mitral valve prolapse and regurgitation Arotic root dilatation >4.5cm = contraindication to pregnancy. If continues pregnancy ELCS >4cm 10% risk of aortic dissection or rupture Give beta blockers (reduces aortic root dilation)

Answer 9

- Pulmonary stenosis - VSD R -> L - Overriding aorta - RH hypertrophy Worsened R-> L shunt. Risk CVA. Fetal ECHO and genetic counselling 2-5% risk (double population)

Answer 10

Asymptomatic Dyspnoea Orthopnoea PND Haemoptysis / pink frothy cough

Answer 11

Mitral facies (flushed cheeks) Cool peripheries Tapping undispalced apex Risk of atrial flutter or fibrillation pulmonary oedema Diastolic murmur

Answer 12

Pulmonary oedema Tachycardia often precipitates this e.g. infection, anxiety, pain, exercise causes a tachycardia, which results in lower filling of left ventricle resulting in lower stroke volume and a build up in pressure

Answer 13

<1cm2 valve area

Answer 14

If severe advise against pregnancy or treat with balloon valvotomy prior to pregnancy Otherwise - ECHO Beta blockers - slow heart so allows time for filling Treat AF aggressively Avoid over zealous IVF Avoid supine and lithotomy pulmonary oedema: treat with oxygen, diamorphine, diuretics

Answer 15

Heart failure that occurs in pregnancy or within 6 months of pregnancy with no other cause known - Diagnosed based on symptoms, high BNP, ECHO <45% LVEF and dilated heart Symptoms: CHF symptoms / signs Risk factors - HTN - Multiples - AMA - Multiparity - Afro-carribean

Answer 16

Elective delivery thromboprohylaxis Diuretics, vasodilators (hydralazine, nitrates), beta blockers, ACEI following delivery 9% mortality If persistent issues with LV size or function, 50% will have worsening HF in another pregnancy and 25% will die.

Answer 17

Type of valve: ball and cage (Starr Edwards) more thrombophilic than new bivalve ones (St Judes) Number of mechanical heart valves Where the mechanical heart vlave is - MV > AV Previous thrombolic events or AF Dose of Warfarin required for therapeutic INR (>5mg = increased risk for fetus) Patient choice

Answer 18

5-10% affected if exposed at 6-9 weeks Nasal hypoplasia and absent nasal bridge Widely spaced eyes Micropthalmia Limb hypoplasis, stippled epiphyses Intellectual abnormality Can switch to LMWH if you want for first trimester Stop Warfarin 10-14 days pre delivery

Answer 19

24h holter sometimes required ECHO to rule out structural disease Only treat if life threatening Digoxin for rate control. OR beta blockers of verapamil (CCB) Adenosine can be used to terminate SVTs (Flecainide if tachyarrythmia in fetus) thromboprophylaxis

Answer 20

Dilated or expanding aortic root >4.5cm Severely impaired LVF

Answer 21

First line oxytocin Then misoprostol or carboprost AVOID ergometrine (Oxytocin should be given slowly if stenotitc lesions or HCM)

Answer 22

* Pulmonary hypertension * Marfans with aortic root dilation >4.5cm MS with aortic valve area <1cm2 * Previous peripartum cardiomyopathy with persistent LV abnormalities LVEF <45% * Unrepaired cyanotic heart disease

Answer 23

Inhibits hepatic synthesis of vitamin K dependent coagulation factors II VII, IX, X and antithrombotic factors C and S

Answer 24

Increased tidal volume Same RR Increased inspiratory capacity Decreased functional residual capacity Slightly decreased TLC increased oxygen consumption < increased ventilation = compensated respiratory alkalosis this increased pO2 to pCO2 facilitates transfer of oxygen to fetus

Answer 25

Engorgment of pharynx, larynx, nasopharynx, trachea Elevation of diaphragm secondary to uterus

Answer 26

PEFr <33-50% of best RR >25 HR >110 Unable to complete a full sentence in one breath

Answer 27

* SABA inhaled or nebulized, 5mg salbutamol * ipratropium bromide 0.5m * IV hydrocortisone 100mg (or oral pred) * IV rehydration * CXR if concern re pneumonia or pneumothorax * admit if PEFR doesn't improve to >75% * Life threatenting: IV beta agonists and MgSO4

Answer 28

If using >5mg prednisone for >3/52 prior to labour. Given 100mg IV hydrocortisone TDS / QID

Answer 29

Misoprostol fine (PG E1) Avoid carboprost (PGF2a - cna cause bronchospasm)

Answer 30

Amoxicillin 500mg - 1g TDS PO + clarithromycin or azithromycin Severe: 1.5g TDS IV Cefurozime + clarithromyin or azithromycin

Answer 31

Viral: decreased Cell mediated immunity - VZV - Influenza - COVID

Answer 32

``` 50% more likely to have extrapulmonary manifestation Course of TB unchanged Safer to treat than to not treat Triple / Quadruple therapy (RIPE) Monthly LFts BF is fine ```

Answer 33

Autosomal recessive, 1:25 Caucasians are a carrier 1:2500 incidence in Australia and NZ Majority of mutations on chromosome 7, CFTR (cystic fibrosis transmembrane chloride channel). Over 1500 different mutations. Most commone delF508 Results in thick mucus in glandular organs and increase sodium in sweat This causes lung infections, bronchiectasis, respiratory failure, pancreatic insufficiency with malnutrition and diabetes / IGT Median age for death is 47 Men are sterile Women are usually fine but sometimes if malnourished or thick cervical mucus - issue with fertility 3 step test for newborn 1. Guthrie - measures IRT (indirect measure of pancreatic injury) 2. elevated IRT --> test for common DNA mutations 3. Sweat test of heterozygous DNA results

Answer 34

Slightly increased mortality rate contraindicated if severe lung disease, chronic hypoxia, pulmonary hypertension Morbidity: worsening lung function (reversible), poor weight gain, infective exacerbation of lung disease

Answer 35

IUGR - esp if hypoxia | PTB 10-25%

Answer 36

1. Pre pregnancy counselling. 1:25 risk of being a carrier. 2% risk of partners risk unknown. Always offer partner carrier testing. If a carrier consider prenatal genetic diagnosis and IVF - Screen for diabetes - Education about expectations - contraindications include Severe pulmonary disease (FEV1 <30-40%), pulmonary hypertension, cor pulmonale (RHF secondary to pulmonary hypertension), recent Burkholderia infection 2. MDT management 3. Adequate maternal nutrition - may need pancreatic enzymes, fat soluble vitamins, dietician invovlement 4. Control of pulmonary infections - Chest physio - Aggressive treatment with antibiotiics and oxygen, sometimes bronchodilators / steroids 5. Avoidance of prolonged hypoxia - May require admission for oxygen 6. Regular growth assessments 7. Delivery plan: aim NVB at term (earlier if deteriorating lung function). Prolonged valsalva can lead to pneumothoraces so offer instrumental 8. BF fine

Answer 37

``` Increased renal plasma flow 60-80% increased GFR / creatinine clearance Increased protein excretion Increased Na and H20 reabsoprtion Increased leukocytes and erythrocytes in urine ``` Dilatation of urinary system (compression and progesterone)

Answer 38

Worsening renal function Worsening proteinuria Escalating HTN

Answer 39

``` Miscarriage PET FGR PTB Fetal demise (urea >20mmol = risk of fetal death, >10mmol = risk of polyhydramnios) ```

Answer 40

Stage 4 and 5 (eGFR <30) | Or Cr >250, especially if on dialysis

Answer 41

1. Pre pregnancy counselling - baseline renal function, proteinuria, BP 2. MDT 3. LDA 4. Treat HTN - aim >110/70 and <135/85 5. Regular bloods: U+Es, albumin, bicarb, Hb, Plt 6. Regular PCR 7. consider Vit D 8. Growth and LV frequently 9. Uterine artery dopplers 10. Admit if worsening kidney function, worsening HTN, PET, polyhydramnios

Answer 42

1. 1 year 2. 95% successful if Cr <125, 75% if >125 Poorer the graft function, poorer the pregnancy outcome

Answer 43

No long term effects | graft rejection 2%

Answer 44

``` HTN / PET 30% FGR 30% PTB 45-60% Infection graft rejection 2% perinatal loss 5% ```

Answer 45

1. MDT 2. BP monitoring 3. Regular renal function tests and PCR 4. FBC / LFTs 5. Anaemia correction 6. Ca ++ (increase or decrease) 7. MSU each visit 8. USS, regular, uterine artery dopplers 9. Maintain level of immunosupressive drugs - prednisone, azathiprine, tacrolimus, cyclosporin fine. Don't give mycophenolate. 10. Admit if deteriorating renal function: ddx. includes renal graft rejection, infection dehydration, obstruction, PET, Calcineurin toxicity (tacrolimus, cyclosporin) 11. Aim NVB 12. If needs CS for obstetric reason consider midline incision to avoid graft, SMO to do

Answer 46

``` Increased liver metabolism ALP increase to ~400, >1000 = abnormal ALT and AST UL = 30 Bilirubin same Increased fibrinogen, transferrin, thyroid binding globulin ``` Decreased gastroic motility and peristalsis decreased lower oesophageal pressure GI motility slows

Answer 47

Thiamine deficiency Symptoms: blurred vision, unsteadiness, confusion, drowsiness SignS: nystagmus, ophthalmoplegia, hyporeflexia, abnormal gait, finger ataxia Associated with a 40% incidence of death!!

Answer 48

1. Wernicke's encephalopathy: Thiamine deficiency 2. Hyponatraemia (central pontine myelinosis if too rapid correction) 3. Vit B6 (pyridoxine) deficiency 4. Vit B12 deficiency 5. Korsakoff's psychosis 6. Mallory Weiss tears 7. Malnutrition 8. Psychology 9. thrombosis

Answer 49

Score for hyperemesis severity Scores 0 -5 based on how many hours nausea, vomiting and dry retching. Max score 15 ≤6 = mild - community management 7 - 12 = moderate - outpatient management 13 and more = severe - inpatient management

Answer 50

HbsAg + HbEAg positive = 70-90% risk, 95% at delivery, 5% transplacental HbsAg +, HbEAg negative = 10-40% risk CS doesn't decrease rates of transmission Given immunoglobulin within and HBV vaccine within 12 hours and vaccine again at 2,4,6 months Can BF 1% of Australian's have Hep B

Answer 51

0.5-1% | autosomal dominant sex linked genetics

Answer 52

LFTs - AST and ALT 3 fold increased, bili sometimes increased, ALP > pregnancy levels, GGT increased, bile acids increased 10-100 times Liver USS - GS Hep B and C (+ hep A, E, CMV and EBV if active symptoms of hepatitis) ONly do smooth muscle antibodies and anti-mitochondrial antibodies if LFT derangement pre-pregnancy or doesn't normalise post pregnancy consider drugs Consider PET and AFLP

Answer 53

``` Maternal: Vitamin K deficiency in severe cases, PPH Fetal - 20% intrapartum fetal distress meconium 30% Spotaneous PTB 15% IUFD (0.13% BS <40, 0.28% BS 40-99, 3.44% BS >100) Fetal intracranial haemorrhage ```

Answer 54

1/7000 - 1/20,000 10-20% maternal mortality rate previous stydies, UK obstetric surveillance system = 2% 20-30% perinatal mortality rate previously, now 11% likely Disorder of fatty acid oxidation (mitochondrial disorder)

Answer 55

Male fetus (3:1) Low BMi Multiple pregnancy LCHAD deficiency

Answer 56

Starts >30/40 with anorexia, malaise, nausea ``` Vomiting (60%) severe Abdominal pain (60%) ``` ``` DIC - 90% postpartum AKI LFTs 3- 10 times Jaundice Lactic acidosis and raised ammonia Risk of fulminant liver failure with hepatic encephalopathy Hypoglycaemia (70%) Symptoms of diabeets insipidus (polyuria, polydyspia) - ADH not cleared ```

Answer 57

Used to diagnose AFLP ``` 6 or more of Vomiting Abdominal pain Raised transaminases AKI Coagulopathy Encephalopathy Raised uric acid Diabetets insipidus Hypoglycaemia Raised ammonia ```

Answer 58

Expedite dleivery MDT + ICU (65% require ICU, 7% require ventilation) Coagulopathy: may need FFP and Vit K hypoglycaemia - treat aggresviely acidosis and raised lactate: poor outcome antibiotics: high risk of sepsis - start tazocin N acetylcysteine - facilitates tissue oxygen delivery desmopression if high UO

Answer 59

5-20% in PET pregnancies 1% maternal mortality 10-60% perinatal mortality rate

Answer 60

TTP, HUS and AFLP rarer Abnormal LFTs and coagulopathy more likely HELLP or AFLP Profound thrombocytopenia (<10) unusual in HELLP or AFLP Hyperuricaemia ++ in AFLP compared to HELLP AFLP - Higher LFTs, hypoglycaemia, hyperuricaemia, leukocytosis

Answer 61

``` Abruption AKI Subcapsular liver haematoma massive hepatic necrosis Liver rupture Death ``` FGR PTB Fetal demise 2-5% risk of recurrence

Answer 62

0.1% Increased incidence as increased production of gallstones in pregnancy secondary to increased concentration of bile cholesterol, slowed gallbladder motility

Answer 63

``` Always confined to colon Watery diarrhoea Lower abdominal pain PR mucus and blood Urgency of defecation ```

Answer 64

Terminal ileum in 30% Ileum and colon 50% colon alone 20% Can affect any part of gGI system from mouth to anus crampy abdominal pain, weight loss, urgency of defecation, sometimes PR blood and mucus but this is more likely in UC

Answer 65

UC - Toxic megacolon - Colon cancer Crohn's - Perforation - Stricture - Malabsorption - fistulae - Fissures / ulcers - Abscesses + extra intestinal manifestations (arthritis, apthous ulcers (CD), gallstones, cholangitis, conjunctivits, erythema nodosum)

Answer 66

UC: 2 x as likely to flare in pregnancy and 6 x as likely to flare postpartum. Exacerbations are usually mild and occur in first two trimesters Crohn's - no more likeyl to flare in pregnancy Highest risk: active disease at time of conception or new diagnosis in pregnancy (can do colonscopy and biopsy in pregnancy)

Answer 67

Active disease: increased rates of miscarriage and PTB Quiescent disease at time of conception: nil risk (Risk of immunosupressive drugs if used into third trimester, baby born with higher levels than mother)

Answer 68

Preconception counselling - Ensure on correct medications. 5 amino salicylates (sulfasalazine) fine but need 5mg folate as sulfasalazine prevents conversion of folate to its active metabolite, thiopurines (azathioprine) fine, TNFa fine (infliximab, adalimumab) - need to stop by 28/40 as active transport to fetus, higher concentrations in neonate then mother at birth if continued into third trimester, corticosteroids fine. Can BF with all meds too - Ensure conceiving when disease quiescent - otherwise increased risk of PTB and miscarriage - Bloods to assess for malnutrition and active disease Antenatal management - If concern re flare: FBC, CRP, LFTs, albumin, stool culture, Faecal calprotection, +/- sigmoidoscopy - Management of attacks same as prepregnancy - MDT approach - Consideration of growth scans especially if active disease - Management to avoid constipation ? - Metronidazole if required for pouchitis Birth plan - Aim NVB unless active perianal crohns disease resulting in rectal scarring / stiffness / deformity. or a rectovaginal fistulae (can do MRI to assess further Postnatal - contact with gastroenterologist if UC as 6 x risk of flare postpartum - All medications required okay with breastfeeding.

Answer 69

Increased thyroid binding globulin synthesis in liver T4 and T3 increased production to compensate TSH increases and then decreases in first trimester Hyperemesis gravidarum can cause a state of biochemical hyperthryoidism - high T4, T3, low TSH State of relative iodine deficiency because 1. Active transport of iiodine across placenta to fetus 2. Increased excretion through kidney because of increased GFR 3. Increased uptake by thyroid because decreased concentration in plasma 4. Hypertrophy of thyroid can occur to trap iodine in it, if dietary insufficiency Fetus is fully reliant of transfer to thyroid hormone until 12/40 when it starts making its own Fetus and breastfed infant is fully dependent on maternal sources of iodine 150mcg / day required in pregnancy and breastfeeding

Answer 70

Thyrotoxicosis normally improves in prengnacy becasue of immunosupression (thyroid receptor stimulating antibodies supressed). - Sometimes have flare in first trimester becasue of HCG and puerperium - Often have to decreased medications

Answer 71

Uncontrolled hyperthyroid results in anovulation and infertility If do get pregnant: increased rates of miscarriage, FGR, PTB, perinatal mortality Thyroid receptor stimulating ab can cross placenta and cause thyrotoxicosis in fetus or neonate: sinus tachycardia, SVT, AF, thyroid storm and heart failure. Mortality in 25% without treatment good control: pregnancy unaffected Both Carbomiazole and PTU cross placenta and can cause hypothyroidism and goitre in fetus. 2-4% risk of congenital abnormalities: Carbimazole > PTU (consider switching to PTU but actually probably better to continue on whatever is working). Check thyroid stimulating antibodies in first trimester - if high for fetal USS Check thyroid function in cord blood once born (and in neonate if mother breastfeeding and taking high doses anti thyroid medications) Look for neonatal thyrotoxicosis: jitteriness, poor weight gain / feeding, hepatosplenomegaly, tachycardia, irritability, goitre, eyelid retraction. Mortality 15% without treatment. Improves after 4 months as antibodies clear.

Answer 72

1% of pregnancies Most common cause is autoimmune thyroid disease - atrophic thyroiditis, Hashimotos 25% will need increase in thryoxine throughout pregnancy Untreated hypothyroidism is assoicated with anovulation and infertility. if do get pregnant assoicated with miscarriage, fetal loss, PTB, PET, anaemia, LBW, perinatal mortality and PPH Iodine deficiency = hypothyroid in fetus = low IQ / neurodevelopmental delay Severe maternal iodine deficiency = neurological cretinism (deaf, mute, spastic) If euthyroid at start of pregnancy maternal and fetal outcome good Only small amounts of thyroxine cross placenta. Check thyroid function each trimester, 4-6 weeks following any thyroxine dose change Decrease dose back to pre-pregnancy levels postpartum

Answer 73

- Check T4, if normal, repeat TSH and fT4 in 4 weeks - Check HCG - Check for molar and multiple pregnancy on USS - Check thyroid receptor antibodies (Thyroid receptor stimulating Ab (GRaves), TPO (risk of postpartum thyroiditis), Hashimotos) o If positive then this may represent subclinical hypothyroidism of an autoimmune origin and so postpartum thyroiditis risk is increased. No evidence of actually treating subclinical hypothyroidism however. - If persistent derangement involve endocrinologist. - USS thyroid if elevated t3/t4

Answer 74

Increased demand for Ca++ in pregnancy and lactation Increased urinary excretion of calcium This means 2 fold increase of calcium absorption from gut is required - vitamin D mediated Vitamin D requirements are increased by 50-100% There is a fall in total serum calcium and albumin but same free ionised form of calcium concetrations

Answer 75

Mother: hypercalcaemia actually improves in pregnancy because of increased demand for calcium from fetus Can get acute pancreatitis + hypercalcaemic crisis, particularly postpartum when fetal demand for calcium is now gone On pregnancy - Miscarriage - IUFD (40% mortality if Ca++ > 3.5) - PTB - PET / HTN - Neonate: tetany, decreased calcium secondary to supressed PTH Treat with surgery unless mild where it can be managed conservatively. Drink plenty of fluids (Hyperplasia or adenoma)

Answer 76

Increase Vit D by 2 -3 fold to increase calcium absorption Increased rates of miscarriage, including second trimester miscarriage Fetal hypocalcaemia, secondary hyperparathyroidism Bone demineralisation and rickets neonatal hypocalcaemic seizures Measure Calcium and albumin monthly

Answer 77

5% NZ | 23% Aus

Answer 78

Deficiency <50nmol/L Insufficiency <75nmol/L risks: Pigmented skin, covered, vegan diet, malnutrition, short interpregnancy interval, obesity, anti epileptic drugs, renal or liver disease, alcoholics

Answer 79

Maternal - Hypocalcemia - Poor bone health - Myopathy - GDM - HTN / PET - SGA - increased risk CS Fetal - Rickets - Neonatal hypocalcaemia with tetany and seizures - Asthma / atopy Management: routine Vitamin D supplementation / day for all pregnant and breastfeeding women (NICE guideline) but RANZCOG: two large quality RCTs hasn't shown consistently improved outcomes. RANZCOG recommendations - Don't test (CNP recommends testing those at high risk, then giving larger doses of vitamin D if low) - Recommend 400IU of vitamin D during pregnancy regardless of risk factors - Advise women about safe sun exposure - Exclusively BF infants should be given 400IU daily of vitamin D for 6/12

Answer 80

renin is released from juxtaglomerular cells (smooth muscle cells in kidneys vessels) in response to low BP, low Na+ (via macula densa cells in distal tubule sensing hyponatraemia and stimulating JG release of renin via PG) and sympathetic nervous system activation to JG cells. This renin then converts angiotensinogen (from liver) to angiotensin I which is then converted to angiotensin II in blood vessels to act on 4 target organs 1. Smooth muscle cells in blood vessels --> vasoconstriction 2. Kidney to cause reabsorption of water 3. Posterior pituitary gland to release ADH which then acts on kidney to reabsorb water and blood vessels to vasoconstrict. 4. Adrenal gland to release aldosterone which then acts on kidney to reabsorb water As a result --> increased BP

Answer 81

Increased renin Increased angiotensin II Increased cortisol (Increased cortisol binding globulin)

Answer 82

Anteiror pituitary enlarges by 35% No FSH / LH Increased Prolactin by 10 times ADH, GH, ACTH all the same

Answer 83

Causes 1. Pregnancy 2. Prolactinoma (macro / micro) 3. Hypothalamic stalk lesions (stopping dopamine inhibition) 4. Hypothyroidism (TSH stimulates lactotrophs) 5. Empty sella syndrome 6. Seizures 7. some drugs (anti - dopaminergic - antipsychotics, metoclopramide) 8. Chronic kidney disease (uraemia--> toxicity to hypothalamus) Pregnancy effect on prolactinoma - Sometimes causes it to grow (macro > micro) - May need to use cabergoline or bromocriptine to prevent further growth - Usually treated prior to pregnancy however as mostly infertile - amenorrhoea Prolactinoma effect on pregnancy - Not usually any issues - Discontinue dopamine agonists in pregnnacy unless enalrging adenoma or symptomatic. - both safe in pregnancy and bf Management Monthly review No need for routine PRL testing No need for routine visual field testing unless symptomatic MRI if symptomatic Check PRL level 2/12 post breastfeeding cessation

Answer 84

Deficiency of ADH, causing inability to concentrate urine Can cause excessive thirst, polyuria, dehydration, seizures

Answer 85

1. Cranial: reduced produciton of ADH e.g. adenomas, destruction of posteiror pituitary, haemorrhage into pituitary, Sheehan's etc 2. Renal: not responding to ADH (CKD, lihtium therapy) 3. Transient: increased vasopressinase by placenta breaks down ADH, or decreased breakdown of vasopressinase by liver (HELLP, AFLP, PET) 4. Psychogenic: increased drinking resulting in polyuria

Answer 86

Exclude other causes of polyuria (diuretic use, hyperglycaemia, hypokalaemia) Admit and document urin output and measure urine and plasma osmolality: if urine osmolality <300 and plasma osmolality >295 and/or Na+ >145 = DI Can give desmopression (doesn't work if nephrogenic) Can give Carbamazepine if renal Advise to drink 20L/day Regular electrolyte measreuements

Answer 87

GH secretion, usually from pituitary adenoma 40% have hyperprolactinaemia secondary to co-secretion or inhibition of dopamine coming down stalk Minimal effect on pregnancy - increases risk of GDM Treat outside of pregnancy only

Answer 88

Infarction of anterior pituitary secondary to massive PPH and hypotension Anteiror pituitary more vulnerable secondary to increase in size Presents with - Failure of lactation - Amenorrhoea, infertility - Loss of axillary / pubic hair - Hypothyroidism - Adrenocorticotropin deficiency - hypoglycaemia, hypotension, nausea / vomiting

Answer 89

``` Pituitary surgery Radiation Sheehans pituitary or hypothalamic tumours pituitary haemorrhafe Lymphocytic hypophysitis (chronic inflammatory cell infiltration, symmetrical enlarged putitary gland on MRI) ``` Low GH, FSH, LH, ACTH, TSH, T4, PRL Replace hormones based on bloods To get pregnant need to use FSH / LH and then pregnancy can support itself after that Otherwise nil effect on pregnancy if appropriately replaced hormones Otherwise can die form hypoglycaemia or hypotension

Answer 90

Overproduction of cortisol <50% from cushing's disease (ACTH production from pituitary adenoma), most from adrenal adenoma / carcinomas Very rare as associated with infertility Dexamethasone suppression test fails to suppress cortisol Effect on pregnancy - Fetal loss - PTB - Perinatal morbidity and mortality - Severe PET - Poor wound healing - NeonatE: adrenal insufficiency secondary to suppression of fetal corticosteroid secretion

Answer 91

Hyperaldosteronism Adrenal adenoma or carcinoma, bilateral adrenal hyperplasia Increased aldosterone = hypertension, hypokalameia, high aldosterone, supressed renin activity Management - Manage HTN Replace K+ Surgery PP

Answer 92

Adrenal medulla tumour that secretes catecholamines 1/50,000 pregnant women Hypertensive crises occur in response to various stress: labour, Ga, opioids, metoclopramide, lying supine Sweaty, nauseated, headahces, palpitations, anxiety, vomiting, HTN, glucose intolerance Diagnose with 24h urine catecholamines Then MRI / USS / CT to find tumour (10% bilateral, 10% malignant, 10% extra adrenal) Effect on pregnany: increased fetal and maternal mortality rate signfiicantly - Fetal 26% in undiagnosed, 11% diagnosed - Maternal 17% undiagnosed, 4% diagnosed Treat with alpha blockade for hypertension and beta blockade for tachycardia for at least 3/7 prior to delivery or surgery (if <23/40) to remove tumour

Answer 93

Adrenal insufficiency usually secondary to autoimmune process. TB can also cause it - Low aldosterone (mineralcorticoid) - Low cortisol (glucocorticoid) Results in hypotension, hyponatraemia, hyperkalaemia and hypoglycaemia and hyperuricaemia Symptoms Weight loss, N, V, Postural hypotension, weakness, lethargy, hyperpigmentation If diagnosed pre pregnancy not usually an issue, just need to uptitrate steroids sometimes Previously had high mortality rate Adrenal Ab can cross placenta but rarely causes neonatal Addisons Management - Hydrocortisone (increased at times of stress) - Fludrocortisone - IV hydrocortisone in labour and wean back to normal dose over a couple of days PP (otherwise can cause profound hypotension)

Answer 94

Excess of androgens, low aldosterone and cortisol High ACTH / CRH (leads to adrenal hyperplasia) Low Na+, high K+ 21 hydroxylase deficiency --> results in high 17OH progesterone and adrenal androgens (95%) 8-9% 11-beta-hydroxylase (does accumulate some deoxycortisol which has mineralcorticoid activity) Causes female fetal virilization secondary to high androgens - Infertile - Amenorrhoea - Salt losing crisis in 21 hydroxylase deficiency - Precocious puberty in a male

Answer 95

Unlikely to get pregnant If do, miscarriage, PET, FGR, GDM increased Ocassionally CS becasue of android shaped pelvis Increased surveillance becasue of PET risk Need to continue on glucocorticoids and mineralcorticoids at pre-pregnancy dose, androgen levels will inform if adequate dosing. Increase corticosteroids if stress including labour

Answer 96

Only will know this is a previous fetus has been affected or know father is affected as well as mother Give dexamethasone from preconception (definitely pre 5/40) to prevent virilization of a female fetus 1/8 fetuses will benefit (autosomal recessive so 1/4 and 1/2 will be female) CVS or NIPT to confirm female, can do microarray to confirm have disease and therefore continue dexamethasone, otherwise can stop it Postpartum all female neonates should recieve corticosteroids and all neonates should have their electrolytes tested at about 24 hours becasue of salt losing crisis Other option: TOP

Answer 97

Pregnancy is an insulin resistant state. Initially in first trimester insulin sensitivity increases and then progressively decreases with increasing gestation Insulin is 2 fold production by the end of the third trimester This is partly due to placental production of human placental lactogen, cortisol and glucagon which all promote insulin resistance glycosuria occurs becasue renal tubule becomes less sensitive to glucose

Answer 98

NZ: 1.12% (0.36 = T1D, 0.75% T2D)

Answer 99

Random venous glucose ≥11.1 Fasting ≥7 2h OGTT ≥11.1 HbA1c >48 on 2 occasions (6.5%)

Answer 100

Increased insulin resistance in pregnancy resulting in increased insulin requirements in type 1 diabetics (usually 2 fold) and often introduction if insulin in type 2 diabetics. Diabetic neuropathy gets worse - sometimes irreversible Diabetic retinopathy risk increases 2 fold Hypoglycaemia more common (tighter glycaemic control in pregnancy) diabetic ketoacidosis can occur more easily. 1-3% risk - BSL >16.3 = risk - If BSL >15 check ketones (>0.6 in urine or >1 in blood = risk so need to treat) Can sometimes even occur when euglycaemic. Symptoms: nausea, vomiting, abdominal pain, fruity breath, increased RR, increased HR, decreased UO, dry mouth, confusion. Maternal ketoacidosis = maternal acidaemia which results in decreased uterine blood flow, decreased placental perfusion, decreased oxygen delivery to fetus - fetal acidosis. Also fetal Hb dissociation curve shifts to right further decreasing oxygen delivery Treat with insulin, IVf, electrolyte replacement and treat underlying cause

Answer 101

Miscarriage risk 2-3 fold PET risk 3-4 fold especially if pre-existing hypertension or nephropathy Diabetic nephroapthy causes severe oedema and normochromic normocytic anaemia Risk of infection Shoulder dystocia Polyhydramnios CS rate 65%

Answer 102

Increased hyperglycaemia in mother --> fetal hyperglycaemia --> icnreased production of insulin from beta cells in pancreas --> hyperinsulinaemia in fetus - Macrosomia - increased oxygen requirement - chronic hypoxia / acidosis - catecholamine release - cardiac remodelling and HTN risk later in life, IUFD risk - Organomegaly - RDS secondary to PTB / CS rate increase also. - Polycythaemia - increased jaundice rates - Neonatal hypoglycaemia - long term neurodevelopmental consequences possible Shoulder dystocia - brachial plexus injury, hypoxia Polyhydramnios from polyuria - PPROM, cord prolapse Increased risk of coengital malformation 4% (2 fold increase) 3 fold increase in NTD and cardiac abnormalities, directly related to HbA!c at the time of conception. Sacral agenesis typically assoicated, also skeletal abnormalities and anecephaly and microcephaly

Answer 103

<18.5: 12 - 18 18.5 - 24.9: 12 - 16 25 - 29.9: 7 - 12 ≥30: 5-9

Answer 104

Pre conception counselling and optimisation of diabetes - Lower the HbA1c the lower the risk of congenital abnormalities - 5mg Folic acid - SCreen for complications: hypertension, nephropahty, retinopathy, coronary artery disease (CARPREG / NYHA), retinal disease, autonomic neuropathy, diabetic foot disease, thryoid disease, coeliac disease, mental health, dental health - ADIPS targets: <6 pre meal, <8.5 1h post meal, <7.5 2h post meal - Review meds - ensure safe for pregnancy - Formally document PCR - Full bloods - Contraindications to pregnancy: IHD, untreated proliferative retinopathy, severe gastroparesis, severe renal impairment (Cr>250) MDT care Early dating and viability Low dose aspirin CAlcium Individualised weight gain recommendation CFTS (some factors altered by diabetes). NIPT - fraction of fetal DNA is altered by weight (50% risk of inconclusive result if ≥160kg) USS 18/40 with fetal ECHO Regular BP and urinalysis (15% chance PET, 50% if nephropathy) Retinopathy review once / trimester 28, 32, 36 weeks Hba1c every trimester ADIPS recommends weekly CTG from 34/40 because of increased risk of stillbirth (7.2 RR (absolute increased risk 1%)) + AFI and USS Lactation consultant review from 32/40 If EFW >4500g and diabetes risk of shoulder dystocia is 20% so offer ELCS Otherwise IOL pre 38+6/40 Pre IOL night before - take normal dose of short or intermediate acting insulin, hald dose of long acting (determir, lantus) Morning of IOL - 50% of any dose of insulin CS: same as above but no insulin morning of Intrapartum: often need sliding scale. Post partum T1d: decrease insulin infusion by half after placenta delivered. Then once eating and BSL 8-10mmol/L SC insulin should be restarted at pre-pregnancy dose or 25-50% lower dose if breastfeeding. T2D: Stop insulin if not on prior to pregnancy. Otherwise drop by 25-40% if itending to breastfeed LIFESTYLE ADVICE Encourage breastfeeding: decreased rates of obesity and diabeted in infants who are breastfed Decreased matenral long term cardiometabolic risks. Discuss contraception and pre conception care.

Answer 105

New England Journal of Medicine 2009 Hyperglycaemia and adverse pregnancy outcomes Looked at risks of adverse outcomes associated with various degrees of maternal glucose intolerance less severe than overt diabetes mellitus 23000 women Bascially just had to do OGTT Primary outcomes - all increased risk with increasing glucose at testing 1. Macrosomia 2. C peptide in cord blood (measure of insulin production in fetus) 3. Neonatal hypoglycaemia 4. CS rates Secondary outcomes also altered 1. Shoulder dystocia and birth injury 2. PET 3. PTB 4. Neonatal jaundice Gave ADIPS cutoffs of fasting 5.1, 1h 10, 2h 8.5 RR 1.75 of adverse outcome Limitations: observation study, doesn't report on confounders such as obesity, gestaiotnal weight gain, previous mode of delivery, previous macrosomia, no cost analysis Strengths: very large study, heterogenous population

Answer 106

Fasting ≥5,1 1h ≥10 2h ≥8.5

Answer 107

NEJM 2005 Does treating GDM improve perinatal outcomes? RCT Intervention: dietician, physician, BSL monitoring, +/- insulin vs placebo blinded if positive for GDM but in placebo arm Primary outcome Serious perinatal outcome composite: shoulder dystocia, bone fracture, nerve injury, death, NICU admission, jaundice requiring phototherapy, IOL, CS, maternal anxiety and depression Secondary outcomes included LGA and macrosomia Outcome RR 0.33 primary outcome Also significant decrease in LGA / macrosomia Treatment improves outcomes Strengths: RCT Limitiation: wide variety of outcomes in perinatal composite outcome

Answer 108

2 moderate or one high risk factor High risk - Previous GDM - PRevious macrosomic baby - BMI >35 - AMA - First degree relative with diabetes or sister with GDM - Previously elevated BSL - PCOS - Corticosteroids or antispychotics Moderate risk - Ethnicity other than European or American - BMI 25-35

Answer 109

Increased risk of shoulder dystocia >4000g No good evidence for IOL - shared decision making principles >4500g and diabetes or >5000g consider ELCS

Answer 110

0.65% Increased significantly with weight 7% >4000g 14% >4500g 21% >4750g Previous shoulder dystocia 7 - 25% diabetic mothers: 2-4 fold increased risk. IOL at term reduces risk RR 0.4

Answer 111

7-20% Erbs palsy 50% - C5 and 6 - adduction and internal rotation Erbs palsy PLUS 35% - C5,6,7 (includes wrist and finger flexion and pronation) Klumpke palsy: C8, T1: Isolated hand paralysis and horners syndrome

Answer 112

1. Reduce bisacromial diameter 2. Increase functional size of bony pelvis 3. Change relationship of shoulder to women's pelvis H - help E - evaluate for epis L - legs - Mcroberts (flexes, abducts, externally rotates) (This plus suparpubic = 50% resolve) P - pressure on suprapubic region E - enter - Rubins II - adduct anterior shoulder - Woods screw - abduct posterior shoulder as you adduct anterior shoulder - Reverse Wood screw - adduct posterior shoulder R - remove posterior arm R - roll Try all for 30 seconds, then try again Then last case scenario - Symphisiotomy - Clavicular # - Zavanelli - Abdominal surgery, hysterotomy and rotate from above

Answer 113

<18.5 12 - 18 <25 12 - 16 <30 7 - 11 <35 5 - 9

Answer 114

Medical complication Risk Gestational diabetes Increased risk to 7% (from 1% BMI 18.5 – 25) Hypertension Increased risk to 10 % (from 2 % BMI 18.5 – 25) Pre-eclampsia Increased risk VTE Increased risk by 10 times T1 or T2DM 3 – 4 % Perinatal death Increased risk to 2% (from 0.5% BMI 18.5 – 25)

Answer 115

10-15% 3-5% (10% of primips) 1% severe PET 0.03% eclampsia

Answer 116

``` 25% PET 50% CS (70% if PET on top) PTB 28% 17% low birth weight <2500g SGA Abruption Perinatal death 4% ``` No recommendation given about IOL. Individualised plan (Always check for other causes of chronic hypertension apart from just "essential")

Answer 117

Cerebral haemorrhage (Secondary to uncontrolled HTN) Multi-organ failure Liver rupture

Answer 118

1. Placental factors - Failure of spiral arteries to remodel as trophoblast invasion is abnormal. this results in abnormal spiral arteries that do not have high capcitence or low resistance. This can result in uteroplacental ischaemia because there is insufficient blood supply to the placenta. Possibly there is also underperfusion of a large placenta e.g. diabetes, multiple pregnancy, hydrops - all increased risk fo PET 2. Maternal factors - PET worsens the pro-inflammatory state of pregnancy - Metabolic disturbance: - Pro-inflammatory cytokines increase, TGs increase. This leads to endothelial dysfunction, increased endothelial cell activation and permeability. Increased cell adhesion molecules on endothelium and prothrombotic factors and platelet activation and vascular tone (decreased prostacyclin synthesis - usually stops paltelet activation and causes vasodilation) (increased thromboxane A2 synthesis - causes platelet activation and vasoconstriction There is widespread microvascular damage which leads to hypertension, proteinuria, hepatic disturbance Anti-angiogenic factors: - VEGF and TGFa normally mantain endothelial health. antiangiogenic factors such as soluble Flt and soluble endoglin are secreted by the placenta in PET ni excess which antagonize these factors Decreased placental growth factor (PlGF) Poor placental development = placental insufficiency – IUGR/SGA -

Answer 119

General - Age >40: 2 fold - BMI >30 : 2 fold Genetic - Mother 25% - Sister 35-40% Obstetric - Multiple pregnancy 2 fold - Previous PET 7 fold - Primip 2 - 3 fold - Long pregnancy interval 2-3 fold with 10 years - IVF, especially with donor egg - Hydrops with large placenta - Molar pregnancy - Triploidy Medical - PRe-existing HTN - CKD - DM - BMI - APS - CT disease - Sickle cell

Answer 120

1. Severe hypertension: Persistent BP >160 despite maximal therapy e.g. 3 agents at maximal doses 2. Worsening bloods: Plt <100, coagulopathy, Cr >90, ALT >70, albumin <20 3. Eclampsia or other crisis 4. Maternal symptoms suggestive of potential crisis: severe headache, epigastric pain, orthopnoea 5. Fetal concerns: severe FGR, absent or reversed EDF on UAPI, placental abruption, fetal distress

Answer 121

Advise tOP Severe maternal morbidity 70% Perinatal mortality 80%

Answer 122

7% | Abruption a risk

Answer 123

Comparing IOL vs expectant management in women with mild Gest HTN or PET, did it affect serious maternal outcomes? Lancet 2009 Multicentre open label RCT Inclusion: singletons, >36/40, no severe PET or other serious comorbidity Number 377 and 397 intervention: IOL within 24h vs expectant management with close surveillance Primary outcome: Composite maternal morbidity - Mortality - Development of severe PET: eclampsia, HELLP, abruption, pulmonary oedema, VTE, >170/110 AN or PN, major PPH Results: significant difference, 29% relative risk reduction, OR 0.58, NNT = 8. No significant difference in mode of delivery or composite neonatal outcome Offer IOL to women with PET post 3740 (Cochrane: 2017: lower risk of composite maternal mortality and severe morbidity in those randomsied to early planned birth RR 0.7, HELLP RR 0.4, severe renal impairment RR0.4. No diff CS rates. Increased risk of NICU admission and RDS)

Answer 124

Contraindicated Teratogenic: cardiac and neurological malformations Renal disease in fetus, oligohydramnios, hypotension IUFD

Answer 125

Resuscitation: A, B, C IV diazepam (2mg/min to max 10mg) or clonazepam may be given while MgSO4 is being prepared if the seizure is prolonged IV MgSO4 loading dose and infusion for 24-48 hours after delivery or last seizure. - 4g loading dose then 1-2g/hour diluted in NS - Side effects: neuromuscular blockade and loss of tendon reflexes, double vision, slurred speech, respiratory depression, cardiac arrest monitor BP, RR, UO, O2 sats and deep tendon reflexes rregularly Serum magnsium levels don't need to be measured routinely unless renal funciton compromised If AKI - same loading dose, but half the maintenance dose. Control of hypertension - aim <160/100 - IV Labetalol or IV hydralazine Delivery once stable!!

Answer 126

``` 1994 Lancet Aim: does low dose aspirin reduce risk of PET and IUGR RCT >9000 women Pregnant with risk factors for PET or IUGR or current concern for PET or IUGR Randomised to aspirin or placebo no significnat change in outcomes - Reduced PEt but not significant Reduced PTB but average of 1 day No signifcant change in birthweight No differnece in SB or NND ``` Cochrane meta-analysis NNT 160 starting <16/40 with those at high risk PET

Answer 127

``` Recurrent PET (15%, 7 fold) Chronic hypertension IHD CVD PPVD DVT CKD Type II diabetes ```

Answer 128

``` PET / HTN in previous pregnancy Chronic hypertension CKD Autoimmune disease e.g. APLS, SLE Type 1 or 2 diabetes ``` ``` OR two of - First pregnancy Age 40 years or older Pregnancy interval more than 10 years BMI >35 FH PET Multiple pregnancy ```

Answer 129

2002 Lancet Does MgSO4 prevent adverse outcomes for owmen with PET and their babies RCT 9996 women ITT, blinded, multicentre MgSO4 loading and maintenance vs placebo Inclusion: pregnant or delivered within 24h, PET, uncertainty whether should have MgSO4 Primary outcomes: eclampsia, death, matneral morbidity Results: halved chance of eclampsia, reduction in mortality but not signficiant, SS reduced placental abruption

Answer 130

1. Medical history: optimise medical conditions and medication use 2. Genetic / FH: offer prenatal screenning for conditions they are at increased risk of: Fragile X, CF 3. Vaccinations 4. Lifestyle recommendations: healthy weight, nutrition, exercise, smoking, ETOH, substance use, iodine, folate 5. Travel and environmental risks 6. Healthy environment

Answer 131

the condition must be 1. Common 2. Have a latent phase 3. Cause significant morbidity and mortality 4. Intervention available 5. Intervention acceptable 6. Cost effective to offer treatment The test must be 1. Voluntary 2. Informed consent 3. High sensitivity 4. Acceptable to the population 5. Diagnostic test available 6. Strategy for managing incidental findings.

Answer 132

1 in 25 -35 carrier, 1 in 2500 -5000 affected cost effective to screen for

Answer 133

X linked condition that causes intellectual disability, behavioural and emotional issues, medical conditions such as epilepsy, MVP, recurrent ear infection, eye issues such as strabismus, physical characteristics: large ears, large testes, long face, high broad forehead, high palate, connective tissue problems ``` FMR1 gene (Fragile X mental retardation protein): trinculeotide repeat increases in copies. >230 = mutation. >55 = premutation. 30 = average unstable, can change in amount of repeats between people ``` 1 in 8000 females 1 in 4000 males

Answer 134

PAPPA and BHCG between 10-12 weeks NT between 11+3 - 13+6 <3.5mm is normal Also adds in age Gives risk of T21, T18, T13 (Increased BHCG and low PAPPa - T21, decreased both T18) Advantages - early screen and therefore early diagnosis - highest detection rate - no added risk of miscarraige - detection of some fetal abnormalities - benefits of early scan: accurate dating, diagnosis of multiple pregnancy, diagnosis of early pregnancy failure Disadvantages - Will detect some affected pregnancies that may spontaneously miscarry - Doesn't provide risk of NTD (but USS will see anencephaly) - Some women may book later - USS: accredited operator - Out of pocket expenses vary

Answer 135

Non invasive prenatal testing Measures fetal fraction of cfDNA and counts chromsomes essentially if more of chromsome 21, concerning for T21 Still a screening test, do >10/40 Need 2-4% of fetal fraction, average is 10% Altered by gestational age (10-12 best), maternal weight (BMI >40? = 50% no result), mosaicism, multiple pregnancy, chromosomal abnormality highly senstivie and specific - both 99%. 45% PPV For t21, 18, 13 and sex aneuploiides Still need 12/40 scan (Can also test for Di-George syndrome and other microdeletion syndromes) Unreportable: 1-5%. Do diagnostic testing, repeat cfDNA, alternative testing) Twins need at least 4% FF to have accuracy - better than CFTS Advantages: - More sensitive and specific - Information on sex aneuploidies also - Don't need technical skill of ultrasonographer, just a blood test - Less strict on timing of test - Can give information on rhesus disease - Better for twins - Can use for single gene disorders e.g. achondroplasia - Overall economic benefit because invasive testing decreased. Disadvantages - Cost - Non reportable result in 5% - Risk of palcental mocaism - Can sometimes give information on maternal conditions e.g. cancer - Still requires invasive testing for confirmation

Answer 136

4 blood tests between 15 and 20/40 Best at 17/40 BHCG (increased in T21, decreased in T18) AFP (decreased in T21, increased in NTD, decreased in T18) Inhibin A ( increased in T21, decreased in T18) Oestradiol (decreased in T21 and 18) picks up 75% of T21 and 85% NTD (when combined with USS 95% NTD) Good for older women - 95% of affected pregnancies will have a high risk result if affected, 50% of pregnancies overall will have a high risk result if <40yo 75% sensitivty 93% specificity 2-3% PPV

Answer 137

Autosomal aneuploidy Non disjunction in meiosis I or II 1:660 - 30: 1:1000, 35 1:300, 40 1:100 (Increases with age, ?because cumulative oxidative stress, depletion in number of normal oocytes available for maturation and shortening of oocyte telomeres Features: wide nasal bridge, epicanthal folds, bracycephaly, webbed neck, upward slanting of eyes, cardiac and / or GI malformations, developmental delay Medical problems: intellectual disability, cardiac malformations, GI malformations, hypothyroidism, epilepsy, respiratory issues, alzheimers, leukaemia, immunodeficiencies Recurrence rates 1 child previously 1:100 >35y = twice the age related risk

Answer 138

1:5000 births Non translocation trisomy aneuploidy not compatible with life Death after 4/7 usually Issues: - Craniofacial malformations - cleft lip and palate - Ocula rmalformations - micropthalmia - Limb defects e.g. polydactyly - Kidney problems: cystic kidneys, hydronephrosis - Cardiac abnormalities - Neurological abnormalities: holoprosencephaly, NTDs - Ventral wall defects such as omphlacoele - Diaphragmatic defects SEVERE intellectual disability if survive (partial or mosaic types) Recurrence risk is very low and almost unknown

Answer 139

``` 1:3000 30% die in one month, 90% die within 12 months Severe developmental delay Severe intellectual disability Cardiac defects urinary and renal tract defects Joint contractures LBW Hearing loss Rocker bottom feet ``` Recurrence rates low and almost unknown

Answer 140

``` 1:2000 45X Webbed neck, cardiac anomalies (coarctation bicuspid AV), renal abnormalities, high arched palate. Primary amenorrhoea Streak ovaries Lack of sexual development at puberty Normal intelligence Short stature Majority mosaic ``` High FSH, refer to paediatric endocrinologist. Can give oestrogen and GH treatments. Frequent otitis media Increased risk of IBD, hypothyroidism, DM

Answer 141

1:500-1000 ``` Tall stature Primary hypogonadism Gynaecomastia Small tests Infertile ``` Delay language Can give testosterone to promote growht of testes, will still be infertile

Answer 142

>11/40 Detects >99% T21 Advantages: can do early so TOP available by curettage, definitive diagnosis disadvantages: miscarriage risk up to 1%, Detects some pregnancis that may have miscarried anyway, 1% risk of equivocal result (maternal cells, mosaicism), 0.1% risk failure to detect (fetal mocasism, not in placenta)

Answer 143

>15/40 (otherwise risk of talipes) 100% pick up of T21 Advantages: 0.5% misacrriage rate only, definitive test Disadvantages: in second trimester, if want TOP need IOL, 0.5% miscarriage rate,

Answer 144

DNA virus Infection 1st trimester: 0.55% chance of congential varicella syndrome, 12-28/40 2%, >28/40 - 0% infectious 48h prior to rash and then until lesions have crusted over Significant risk: 5 mins face to face, living with someone or ins ame room for >1h 1. Define maternal exposure previously - IgG positive = immune. IgG negative = at risk 2. risks to mother : pneumonia (5% mortality), neurological manifestations 3. Risk to fetus: congenital varicella syndrome or neonatal varicella 4. Expsoure <96h --> give ZIG, exposure >96h - no ZIG, Consider aciclovir if high risk 5. Chicken pox develops: ≤24h since onset of rash: oral aciclovir, >24h no aciclovir, complications or immunocompromise IV aciclovir 6. FM counselling - USS 5/52 post chickenpox - features of varicella zoster syndrome: skins carring 78%, eye (60%), neurological, limb, gut, prematurity / LBW 7. Routine scanning following this. No need ofr amniocentesis but can sometimes be useful to know PCR result. 8. Only delivery if fetal compromise of unable to ventilate mother because of gravid uterus. 9. Chickenpox <7 days before to 2/7 after delivery: ZIG to neonate immediately! 10. Chickenpox >2-28 days post deliveyr given infant ZIG if <1000g or <28/40 gestation. 11. Breastfeeding encouraged.

Answer 145

DNa herpes virus Most common congenital infection Testing - IgM + , IgG + (diagnosis of new infection if previously IgG negative) - IgM - , IgG+ = past infection - IgM +, IgG - = very recent infection or false positive. repeat 2/52 - IgM +, IgG + low avidity = recent infection - refer FMM, amnio 6/52 post infection and >20/40 (otherwise very poor sensitivity) - IgM +, IgG + intermediate avidity = probable recent infection = refer - IgM +, IgG + high avidity, recurrent infection = refer 30-40% risk of transmission in utero 10-20% risk long term sequelae 10-15% symptomatic congenital CMV (50% long term sequelae) 85-90% asymptomatic at birth: 10-15% long term sequelae Detection of virus is high from aniotic fluid as fetus urinates the virus out In utero: oligo / poly, cerebral calcifciaitons, microcephaly, hydrocephalus, IUGR, hydrops, heaptopmegaly etc etc etc Birth: early mortality (3/12), microcephaly, seizures, developmental delay, chorioretinitis, sensoineural hearing loss Prevfention better than cure!!: high risk parents and people working at daycare.

Answer 146

Gram positive rod Aerobic and facultatively anaerobic. Grows at 4-10 degrees Predilection for placenta and CNS pregnant women susceptible because decreased T cell funciton and predilection of placenta Transmission highest in 3rd trimester, 70-90% of foetuses get infected, 50% mortality Non specific illness (diarrhoea, fever, flu like illness, meningitis, 1/3 asymptomatic) Fetus: mec liquor <34/40, PTB, granulomatis infant septica, neonatal late onset disease (sepsis / meningitis Do blood cultures If positive: Amoxicillin 2g IV q6h 2/52 AND gentamicin If allergy: erythromycin and cotrimoxazole (not in first trimester) AVOID high risk foods and use safe food handling practices

Answer 147

Single stranded DNA virus Transmitted by respiratory droplets Infects erythrocytes precursors and causes fetal death, anaemia and hydrops - Suppression of bone marrow 40% of women are non immune 50% of those infected will have fetal infection 10% miscarriage <20/40 3% hydrops - If hydrops 30% resolve, 30% die if no IUT, 30% resolve after IUT, 6% death after IUT - No need for amnio - If positive for parvovirus (i.e. IgM and IgG positive), need 2 weekly scans for MCA PSV and hydrops for 12/52, then can stop if normal result.

Answer 148

Togavirus Incidence low secondary to MMR vaccine Direct droplet spread versus haematogenous spread through placenta <12/40: 80% risk fetal infection, 85% CRS 13-16: 50% fetal infection, 35% CRS 17- 30: 30% risk fetal infection, CRS rare 30-36: 60% risk fetal infection, CRS rare >36:40: 100% risk fetal infection, CRS rare ``` CRS Triad: cataracts, deafness, cardiac defects (PDA, pulmonary artery bracnh stenosis) Microcephaly IUGR, IUFD, PTB Interstital pneumonia Hepatsplenomegaly Blueberry muffin spots Developmental delay etc etc. ``` IgM and IgG positive, repeat to confirm and then counsel (positive) First trimester: TOP Can do CVS and amnio (best if >6/52 post infection and >20/40): PCR, culture, fetal IgM (can get false psoitive with CVS becasue of matenral tissue) At birth test IgM, PCR and culture for baby Born with clinical features of Rubella: IgG ≥ maternal IgG, IgM +, PCR +: Ophthalmology and hearing 3-6/12 assessments, infants infectious 12/12.

Answer 149

Protozoan parasite From undercooked meat, cat litter, placental transfer, unwashed salads Lies dormant, never clear it Problem if immunocompromised or get it for first time in pregnancy 1st trimester: 10% chance of fetal infection, 90% chance of fetal damage 2nd trimester: 45% and 20% 3rd trimester : 90% and 10% Causes calcifications in liver and brain, ventriculomegaly, non immune hydrops Exposure: check serology - 2 blood samples 2 weeks apart - IgM negative, IgG negative no primary infection - IgM negative, IgG positive, infection >2 years ago - IgM + and IgG negative, infection within last 2 weeks - IgM +, IgG + low avidity: infection within 12 weeks - IgM +, IgG + high avidity: infection >12 weeks ago Refer FM uni Amniocentesis for PCR (must be >18/40 and >4/52 from infection) Spiramycin if <18 / 40 if mother exposed If confirm fetal infection or more than 18 weeks given pyrimethamine and sulfadiazine and folinic acid. Classic triad: chorioretinitis, hydrocephalus, intracranial calcifications. Visual loss if untreated.

Answer 150

Spirochete Incidence rising, 500 cases last year in Aus Primary: chancre Secondary: palms and soles rash, lethargy, fever, malaise, hepatitis, etc. Early latent <2y: asymptomatic Late latent: >2 y since acquisition, asymptomatic Tertiary: cardiovascular, neurological abnormalities, gummas (soft tissue growths) EIA first, if positiv,e TPPA, if positive RPR to assess disease activity Other STI checks Contact tracting: symptom duration + 3/12 if primary, 6/12 if secondary, 1 year if latent, long term partners if teritary syphilis in pregnancy: miscarriage, stillbirth, SGA, LBW, Congenital syphilis: - Primary: up to 100% - Secondary: up to 100% - Early latent 40-80% - Late latent: 10% - Hepatosplenomegaly, poly, ascites, anaemia, bowel dialtion, long bone abnormalities, IUGR (Late congneital syphilis - untreated or inadequately treated: teeth abnormalities, bone abnormalities, keratitis, neurosyphilis, hearing loss) Neonate diagnosis: RPR 4 fold higher than mothers, TPPA positive after 18/12, RPR or VDRL positive after 6 months. Successful maternal treatment: 4 fold decrease in RPR, check every 4 weeks. Give benzathine benzylpenicillin tetrahydrate 2.4mU IM once if primary ro secondary, 3 x (weekly) if latent or tertiary Jarisch Herxheimer reaction 45% (admit if viable gestation)

Answer 151

Streptococcus agalactiae Colonisation in 10-30% of women 50% of babies will become colonised when born ot these mothers, 1-2% will have EOGBS, fatality rate is 15%, 20 x this in preterm babies Intrapartum antibiotics decrease EOGBS by 80%, doesn't change incidence of late onset GBS EOGBS: pneumonia / resp symptoms LOGBS: meningitis, septicaemia NNT 224 0.4 - 4/1000 live births EOGBS without antibitoics Risk factors - <37/40 - Previous baby with EO or LOGBS - GBS in urine earlier in rpegnancy - GBS on swab in pregnancy - Prolonged ROM >18h - Maternal fever ≥38 - Chorio - Other twin with EOGBS RANZCOG supports with universal screening at 35-37 weeks or 3-5/52 prior to anticipated delivery with anorectal and vaginal swab, enriched culture media, specify GBS screening, and specify if allergy to pencillin so can do clindamycin resistances (20%) and erythromycin resistances (30%). OR risk factor based screening Give penicillin in labour Cefazolin if allergy Clindamycin or erythromycin if anaphylaxis Vancomycin if resistance to clinda and erythromycin PPROM - IOL form 34/40 ROM at term - immediate IOL and IAP.

Answer 152

Incidence in Australia 1% Sexual, blood and vertical Universal testing in pregnancy because 50% of people don't know they are chronic carriers HbsAg positive - reflex liver USS, HBsAb, HBeAg, HBeAb, HBcAb, LFTs, prothrombin time HBsAg + = active infection - acute or chronic HBsAb +, HBsAg negative: immunity HBcAb: past or current infection HBeAg: immune tolerance or immune clearance - high risk of vertical transmission if positive = 70-90% risk vertical transmission HBeAb + = viral clearance or immune control. HBV DNA >10to7, give tenofivir from 30/40 and do ALT 4 weekly, if <10-7 don't Don't breastfeed on tenofivir. HBsAg and HBeAg positive: 70-90% verticla transmission risk. 95% vertical, 5% transplacental. CS doesn't decrease rates. If infected at birth 90% risk chronic carrier (high risk cirrhosis and Hepatocellular cancer). GIVE HBIG and HBV vaccine within 24 horus of birth. HBV vaccine can be given up to 7 days Give further vaccine at 2,4,6 months. Serology 9/12 of age HepB acutely in pregnancy: if HBsAg <10IUml give hep B vaccine and HBIG wihtin 72h. Retest 3/12.

Answer 153

RNA virus Transfusion prior to 1992, IVDU, Sex (uncommon) RANZCOG: 1% of women in childbearing years 3-5% risk MTCT Mostly vertical transmission at birth, and confined to those with positive RNA high levels or HIV co-infection (20%) Measure Hep C Ab in all women, if positive measure HCV RNA and LFts. If HCV RNA negative oculd mean false positive Ab, very low viraemia secondary to treatment or cleared infection, or just very low viraemia Avoid invasive procedures CS no benefit BF okay unless cracked bleeding nipples Infant born: wash before any injections. Measure HCV RNA at 3/12, if positive another positive test 3/12 later confirms. Otherwise can measure Ab at 18/12 to confirm Maternal: no treatment during pregnancy or rbeastfeeding. Can treat with Marivet afterwards (DAAT): 95% cure rate.

Answer 154

A, B, c (A is the worst) Orthomyxoviridae family Pregnant women more at risk becasue of altered lung funciton, increased CO, increased oxygen consumption, alterations in immune function. Doesn't cross placenta but can cause congenital abnormalities (cleft palate, NTD, cardiac) or miscarriage, PTB, IUFD from the hyperthermia / maternal unwellness Influenza vaccine safe in all trimesters (inactivated vaccine) Maternal benefits: 50-80% reduced risk in influenza, 40% reduction in hospitalisation. Fetal benefits: 27% reduced risk in stillbirth, 13% reduction in LBW / PTB, Neonate: 40% reduced risk in infant death and hospitlisation from respiratory infections <3/12 of age

Answer 155

HIV1/2 Lentivirus Retrovirus Low rates in NZ / aus Antenatal screening universal - HIV Ab positive (ELISA then Western blot) - If positive measure HIV RNA< CD4+ count, HIV resistance testing, full STI screen, FBC, U+Es, LFTs - If positive need physician input, MTCT counselling. - If negative but high risk recent exposure, remeasure 4/52 MTCT <2% if HIV RNA undetectable, on HAART, appropriate mode of delivery, formula fed baby with PEP MTCT 20% if optimal measures not in place and 40% if breastfed HIV+ and conceived on HAART with undetectable viral load at 36/40: vaginal birth fine, no need for IP zidovudine, formula feeding and PEP HIV+ and naiive to HAART but needed for maternal health start ASAP (Zidovudine and lamivudine are most common combinaiton therapy). If VL <50 copies / mL at 36/40 as above If VL >50 copies / ml but less than 400 copies / mL: Consider IP Zidovudine and CS at 38-39/40. Formula feeding and PEP If >400 - IP Zidovudine and CS recommended 38-39/40. Formula and PEP If naiive to HAARt but doesn't need for own health still start pre 24/40 IF late presenter with no HAART - Not in labour >28/40: Give HAART asap, IP Zidovudine, CS, formula, PEP - If VL really high need extra combination therapy required - If presents in labour at term: Start combination therapy asap. CS If pre-term: Start HAART combination asap. Mode of delivery dependent on obstetric factors Baby: PEP immediately, monotherapy if low risk, combination therapy if high risk. Serology follow up till 18/12. Formula feeding.

Answer 156

4 subtypes Transmitted by anopheles mosquito 1500 cases / year in UK, 0.5 - 1% mortality rate Replicates in liver then comes out into blood and infects erythrocytes, which then stick to small blood vessels in brain, kindey, lungs etc. Interferes with microcirculation, flow and metabolism. Sequesters in the placenta and evades host defence mechanisms, splenic processing and filtration. This results in poor oxygen transfer and FGR, LBW. Can cross and infect fetus causing fetal anemia Cyclical fevers, non specific unwellness. Severe malria: cerebral oedema, severe haemolytic anaemia, ARDS, coagulopathy, cardiovascular collapse, kidney failure, metabolic acidosis Admit - To ICU if severe - Treat with quinine and clindamycin if not severe, artesunate if severe. - Only delivery if fetal distress or failure to treat woman appropriately - consider thromboprophylaxis if plt >100 risks - Severe febrile illness: maternal and fetal mortality, SB, premature birth, miscarraige - Parsitatisation: FGR, LBW, fetal anaemia

Answer 157

Bordetella pertussis Highly infectious bacteria - gram negative coccbacilli Babies are vaccinated 6/52, 3/12 and 5/12 of age. Vaccinate between 20 -32 weeks (or anytime) but transfer of immunity occurs 2/52 form vaccination Acellular vaccination, safe in pregnancy. Recommend repeat vaccination in each pregnancy Infectious until completed 5 days of antibiotics.

Answer 158

Flavivirus Transmits via mosquito, or sex, vertical transmission, blood transmission High endemic areas: south america, central america, africa, indonesia, part of SEA Fever, arthralgia, headache, conjunctivitis, myalgia, rash etc... No evidence pregnant women are more susceptible to the virus or seriousness of disease Ix <2/52 since exposure: RNA PCR urine and blood >2/52 or negatibe RNA: test IgM. If positive confirm with PRNT. (+negative PRNT for dengue) USS: microcephaly, intracranial calcifications, multiple other cranial abnormalities, oligohydramnios, talipes, FGR ~15% transmission of zika transplacentally. First and second trimester much higher risk of congenital zika syndrome 4/52 USS Consideraiton MRI Consideration amnio if >20/40 and more than 5/52 and uncertain if condition secondary to Zika (although doesn't confirm causality) Pretravel: avoid travel to high risk areas Travel: avoid mosquitoes, and UPSI Post travel - Avoid UPSI for duration of pregnancy or 6/12 if a male partner has travelled (Zika can live in sperm for up to 6/12) - Avoid UPSI for 3/12 if both partners travelled OK to BF

Answer 159

Risk of neonatal herpes - 3 types - Eyes, skin, face only. 30% of cases. Good prognosis if treated - CNS - Disseminated CNS and disseminated - 30% mortality with antivirals. 17% long term neurological sequelae Congenital herpes VERY rare 50% HSV1, 50% HSV2 cause neonatal herpes HSV in pregnancy - Recurrent episode: ensure is not a new strain (swab and serology). If not a new strain, give suppressive therapy (e.g. valaciclovir 500mg BD 3/7). Suppressive therapy from 36/40. Time of labour speculum to ensure no active lesions. If active lesions 1-3% risk of transmission (HSV 1 15%, HSV 2 0.01%), individualised discussion. No active lesions NVB fine. Avoid FSE, instrumental, FBS - New episode 1st and second trimester. Swab and serology. Given 5/7 valaciclovir 500mg BD and then from 36/40 . OK for NVB. As per recurrent episodes. Screen for STIs - New episode third trimester. Swab and serology. Give 5/7 valaciclovir and then from 36/40. Check serology 36/40 to ensure seroconverted, if seroconverted then NVB okay as long as no active lesions. If not, CS recommended as risk 25-50% of transmission. - If primary episode within 6/52 of labour CS recommended - If SROM with active lesions or primary episode within 6 weeks CS recommended - If first episode in labour: CS recommended. If declines 20mg/kg aciclovir IV in labour. - PPROM with first episode: MDT discussion. Given 24-48h aciclovir IV while steroids given - PPROM recurrent episode: expectant management appropriate - give oral aciclovir 5/7 and then from 36/40 Risk mother getting unwell: disseminated HSV, hepatitis Neonate: - Low risk: swabs and PCR at 24h - High risk (primary genital or systemic herpes close to delivery, or infant born through birth canal with active HSV disease to mother with no history of HSV): full septic screen and give aciclovir immediately from birth

Answer 160

``` T = tolerance A = annoyance at others commenting on your drinking C = cut down - feel like you need to cut down E = eye opener (need a drink to start your day) ```

Answer 161

Social: homelessness, prostitution, violence, trauma, criminal activity, family disruption Medical: infections, neurological, CVS, resp, mental health, poor nutrition / dental health / skin Psychological: 60-80% psychiatric comorbidity, depression, anxiety, mania, drug overdose, abuse, low self worth, self harm, eating disorders, inability to care for children obstetric risks: miscarriage, neonatal or IUFD, abruption, anaemia, needs for pharmacological alterations in birth and postnatally, congenital abnormalities Neonatal: LBW, neonatal abstinence syndrome, increased risk of prematurity, increased NICU admission, child protection issues, SIDS

Answer 162

``` Triad - Facial characteristics - Growth retardation - CNS / brain abnormalities Difficulty transalting sensory modalities into action (e.g. reading into speaking), difficulty generalising information, difficulty perceiving similarities and differences ``` Also heart, kidney, hearing, eyesight, skeletal, immune system Part of fetal acohol spectrum disorder (FAS, partial fetal alcohol syndrome, alcohol related birth defects, alcohol related neurodevelopmental disorder) 2/1000

Answer 163

11% of Australians smoke Carbon monoxide binds to Hb and diminshes oxygen carrying ability Cadmium accumulates in placenta, is a carcinogen, and reduces fetal capillary volume Nicotine interfers with amino acid transport across the placenta and results in LBW, PTB, IUGR Also - spotnaeous abortion - ectopic - Placental abruption - PROM - Behavioural problems - Lung issues - SIDS - Altered critical autonomic reflexes

Answer 164

THC crosses placenta and is present at 10% higher concentrations in fetus than mother Neurodevelopmental deficit No effect on BW No teratogenicity

Answer 165

Rapidly crosses placenta Peaks and troughs in blood Anaemia, IUGR, Preterm labour, decreased pain threshold, neonatal abstinence syndrome

Answer 166

Benefits - Partial mu receptor agonist, so less likely to OD or have resp depression - Neonates recover faster from neonatal abstinence syndrome - Can BF - Fewer drug interactions than methadone Reduces preterm birth and low birth weight. Buprenoprhine better than methadone at this Risks - Hepatic dysfunction lack oflong term data

Answer 167

Binds to opioid receptors blocking them so no effect from other opioids Also binds to NMDA receptors which contributes to pain relief. Stops craving and withdrawal symptoms Dose needs to be icnreased in pregnancy Interacts with lots of other drugs including antiretrovirals Reduced preterm birth and low birth weight

Answer 168

High pitched crying, feeding issues, GI disturbance, irritability, yawning, sneezing, increased RR, low grade fevers, seizures, failure to thrive, death Treat with liquid morphine Severity doesn't correlate with dose of Buprenorphine or methadone Severity is reduced with rooming in, BF, skin to skin

Answer 169

``` increased synaptic dopamine, serotonin and noradrenaline and blocks reuptake Increased risk of psychosis Large cross into breastmilk Neurobehvioural difficulties Probably PTB and LBW rates higher ``` alertness, elevated mood, increased sustained attention, supressed appetite, increase HR and BP, MI, Arrhythmias, dilated pupils, sweating, hyperthermia, tremor, hyper-reflexic slurred speech, agitation, obsessive behaviour, delirium, psychosis

Answer 170

``` - Cocaine use can lead to placental abruption and fetal or neonatal cerebrovascular events. Appropriate consultation or referral is recommended o IUGR o Intrauterine hypoxia o Preterm labour o Placental abruption o IVH o Neonatal cerebral infarction o Brain lesions o NEC o Euphoria o Effects on dopamine receptors ```

Answer 171

Major - Medical condition: SLE, APLS, Diabetes with vascular disease, hypertension, renal disease - Maternal age >40 - Smoker >11 / day - Bleeding heavy enough to be menses - PAPP-A <0.4 MOM - Paternal SGA - Maternal SGA - Previous SGA - Previous stillbirth - Cocaine - Daily vigorous exercise - Fetal echogenic bowel Minor - Previous PET - Low fruit intake pre-pregnancy - Age >35 - IVF - Nulliparity - >60 months between pregnancies, <6 months between pregnancies - Smoker 1 - 11 - BMI <20 or >25-35

Answer 172

SGA with normal dopplers - by 40/40 (RCOG says 37/40???) Unless - >34/40 and static growth over 3 weeks. Abnormal UAPI with positive end diastolic flow or abnormal MCA - 38/40 Abnormal UAPI with absent end diastolic flow and >32/40: by 34/40 Abnormal UAPI with reversed end diastolic flow: 32/40 <32/40 deliver when DV abnormal (MCA: 55% risk CS) (Very abnormal uterine artery dopplers, risk of delivery pre 34/40 is 60%)

Answer 173

Lancet 2015 Multicentre prospective RCT 500 women Europe 26-32/40 with FGR (AC <10th with abnormal UAPI), >500g, no delivery plan or fetal anomly, normal DV and normal STV, no karyotype abnormlaity, >18y o 1:1:1 - STV (daily CTG) <3 (26-29), <4 (29-32), Early DV changes (>9th), Lat DV changes (absent or reversed A wave) - twice weekly scans Safety: STV <2.6 or <3, maternal reason for delivery Primary outcomes: survival at 2 years without cerebral palsy, neurosensory impairment or Bayley III score <85 Secondary outcomes: death or severe neonatal morbidity No difference If take away the deaths in favour of late DV changes 92% survival 2% IUFD 6% NND

Answer 174

Maternal: comorbidities such as PET, ESS HTN, collagen vascualr disease, nephropathy, thombophilia, or medications such as ACEI Placental: Abruption, TTTS, Placental thrombosis or infarction Fetal: chromsomal abnormality (T13 and triploidy most common), congenital abnormality (e..g urethral atresia, posterior urethral valves), growth restriction, infections, demise, ROM, Postterm pregnancy Idiopathic

Answer 175

<26/40: poor prognosis. 30% will have severe pulmonary hypoplasia, of which 70-90% will die. 26/40: canalicular stage of lung development, after which lungs are less sensitive to external pertubations - If die likely from infection, cord compression or uteroplacental insufficiency which is causing the oligo <20/40

Answer 176

Fetal - Anything that impairs swallowing: brain abnormalities (Dandy Walker, Anencephaly), facial tumours, GI obstruction (duodenal atresia, oesophageal atresia), large pulmonary abnormalities such as diaphragmatic hernia, CPAM - Multiples: TTTS - Anaemia: hyperdynamic circulation = increased uriantion Maternal - Diabetes - Lithium use - Infections: parvo, CMV, Toxo, Syphilis, Rubella - Hypercalcaemia Idiopathic: most common

Answer 177

normal 8-24cm Mild 25-30 Moderate 30-35 Severe 35 Overall perinatal mortality raised, 2-5 fold compared to normal fluid.

Answer 178

Ectoderm: skin, nervous system Mesoderm: connective tissue, bone, muscles, urogenital organs, pleura, peritoneal linings endoderm: lining of internal organs such as GIT and lungs

Answer 179

Week 3 from conception neuralation starts. Ectoderm starts to form neural crest and neural groove (neurulation - stimulated by notochord). Folds over and forms neural tube by end of weeks 4. Rostral end closed by day 25. Caudal end by day 27.

Answer 180

``` Folate deficiency (poor diet, poor absorption, genetic factors that decrease absoprtion / metabolism, Folic acid antagonist (valproate, carbamazepine, methotrexate) Genetics Chromsomal abnormality Syndromes: T12, T18, limb body wall complex, triploidy, Meckel Gruber Fever Amniotic bands pregestational diabetes obesity (2 fold) ```

Answer 181

``` Lemon sign: abnormal frontal bones Banana sign: hypoplastic cerebellum Ventriculomegaly Splayed lateral pedicles Bulge at lumbar spine- Talipes – movement problems -Scoliosis Direct signs: spine - Looking at vertebral bodies and cystic structure - Gibbus – sharp bend in spine – poor prognosis ```

Answer 182

``` Presence and severity of brain signs Presence of other abnormalities: 20-30% Chromosomal / genetic abnormalities: T18 Gestation at delivery Birth weight Level of lesion In utero limb movements ```

Answer 183

Surgical - Operation within first 24h - Most need shunt < 1 year of age Mortality - 25% SB - Can die in first year of life secondary to hydrocephalus or infection - After first year most common cause of death renal failure Mobility - Depends on level of lesion Intelligence - Most normal or near normal Continence - 25% both continent - 40-85% incontinent of 1 Sexual function can be altered Psychosocial - Most report good quality of life

Answer 184

<4% unless genetic component HIGH folate next pregnancy and 12 and 16/40 USS Affected parent or one siblibng 5% two affected siblings 10%

Answer 185

5-20/10,0000 births | Anencephaly PRE folate 1/1000

Answer 186

Failure of rostral pore to close by day 25, results in no cranial ossification Neural tissue exposed to CSF, necrosis occurs Face normal 10% chromosomal abnormalities 50% other anomalies Incompatible with life - IUFD, poly, preterm labour, NND Recurrence - 1 affected sibling 5% - 2 affected siblings 10% Reduced risk by 75% if folic acid

Answer 187

Echogenic areas in bowel equivalent to bone 1% in second trimester (1st trimester can't tell, 3rd trimester = not clinically significant) Non specific USS finding Can be associated with increased risk of chromosomal and non chromosomal fetal abnormalities (35%) Possible pathology: inspissated meconium, decreased vascaulrity, bowel hypotonia, swallowed blood 3-25% risk of aneuploidy CF - 3% intra-amniotic bleeindg and swallowing of blood congenital malofrmation of bowel: atresia, proximal obstruction, perforation, hirschprungs, meconium peritonitis IUGR with increased risk perinatal morbdiity and mortality congenital infection (CMV), Toxi ``` Anomaly scan Amnio (karyotype, PCR for virology, DNA analysis for CF) OR cfDNA Maternal virology screen - toxo, CMV prenatal CF screen for carrier status ``` Management - if ruled out everything else increased fetal surveillance: monthly growth scans (increased risk of IUGR and IUFD)

Answer 188

``` Cysts in lateral ventricles >2mm 90% resolve by 26/40 Present in 2% of fetuses at 20/40 most spontaneously resolve and are benign associated with T18 and T21 ```

Answer 189

When varies by >4/7 from a scan performed 6-13/40 (most accurate time) If cycle not regular If LMP not certain

Answer 190

GS 5/40 GS+YS 5.5/40 GS + YS + emrbyo too small to measure 6/40 FH 6.5 - 7/40 (MSD + 30 = GA is 5-11/40) (CRL + 42 = GA is 6- 9.5/40) Fetal pole should grow by 1mm a day at 5 7 weeks

Answer 191

initial scan: 1. No FH when CRL >7mm 2. no YS or embryo when MSD ≥25mm On FU scan 1. No FH when previously FH was seen 2. MSD ≥12mm with no embryo and a repeat scan shows no embryo or yolk sac after 7 days 3. CRL <7mm, no FH after 7 days 4. MSD <12mm with no embryo and there is no yolk sac or embryo after 14 days 5. If YS seen on initial scan but there is no embryo with a FH after 11 days

Answer 192

Initial scan - CRL >7mm no FH - MSD >25mm no YS Repeat scan - FH no longer when present earlier - CRL <7mm, scan in 7/7 shows no FH - MSD >12mm, scan in 7/7 shows no YS or embryo - MSD <12mm, scan in 14/7 shows no YS or embryo - MSD with YS, scan in 11/7 - no FH

Answer 193

``` CSP Falx Thalami No orbits No posterior fossa ```

Answer 194

``` Stomach Left and right portal vein continuous (J) one single rib No kidney No lung ```

Answer 195

cartilaginous femoral head and epicondyle

Answer 196

Day 2 of life Senstivie to oxygen (low oxygen = PDA), PGs (high PGs = PDA) (PG concentration inversely proportional to O2), and bradykinins (increased as increased blood flow through lungs)

Answer 197

Fetus Adult Ductus vensosus Ligamentum venosum Foramen ovale Fossa ovalis Ductus arteriosus Ligamentum arteriosum Umbilical vein Ligamentum teres Umbilical artery (2) Medial umbilical ligament (2) + superior vesical artery Allantois Median umbilical ligament

Answer 198

D (15% of people are rhesus negative and 16% will make Ab if make a rhesus +ve fetus, with no intervention) K (E +c) c (Also duffy, jka, Kidd) Kell kills becasue - haemolysis from IgG Ab crossing the placenta - Fetal bone marrow erythropoiesis suppression leading to aplastic anaemia - severe fetal anaemia can occur at even relatively low titres Clinically significant Ab test every 4 weeks until 28/40 and then 2 weekly (D, K, c +/- E) Other Ab retest at 28/40 unless hx HDFN

Answer 199

D: >4IU/mL (Refer at 1:16 to 1:32 depending on local threshold), >15IU/mL = risk fo severe HDFN K: immediately c: >7.5IU/mL (>20IU/mL = risk of severe HDFN E: immediate if c present Do paternal genotype or NIPT If paternal genotype negative (i.e. dd or kk) no NIPT / testing required If paternal genotype heterozygous need NIPt (>16/40 and >20/40 for K) If paternal genotype homozygous then fetus is at risk of HDFN, refer to FMM for USS, MCA, +/- IUT DELVIER 37/40 (39/40 if titre remains under critical titire) Cord blood: Hb, DAT, Bili Also refer to FMM if unexplained severe neonatal jaundice or anaemia requiring transfusion in last pregnancy OR a history of HDFN or IUT or any of the Ab >1:32 titre, especially if rising FMM will do weekly MCA PSV if above titre thresholds or K Ab. If >1.5MoM or other signs of fetal anaemia (poly, cardiomegaly, skin oedema) for invasive treatment - FBS and IUT MCA PSV is predictive of moderate to severe anaemia with 100% sensitivity and a 12% False positive rate After 36 weeks not as good. Risk of fetal loss after FBS is 1-3%, higher if hydrops If first pregnancy had severe anaemia, then just start doing MCA PSVs from 16-18 weeks as the Ab titres don't reliably predict the severity of fetal anaemia. (OR 10/52 prior to poor outcome)

Answer 200

``` Give type O or ABO compatible if known Cross match compatible with maternal plasma and negative for relevant antigen. K negative to ensure no future issues <5 days old Citrate phosphate dextrose anticoagulany CMV seronegative Irradiated and transfused within 24h ``` WE are giving adult Hb which means it doesn't bind oxygen as well!

Answer 201

reduced alloimmunisation by 78% Give 1 vial for every 6 mL fetal RBC in maternal blood If more than 2 vials needed disucss with transfusion specialist Mechanism of action unknown: possible rapid clearance of anti-D coated D positive red cells by macrophages and down regulation of antigen specific B cells

Answer 202

Accumulation of abnormal fluid in at least 2 different fetal compartments - subcutaneous oedema - pleural effusion - pericardial effusion - ascites - placental thickening >6cm - polyhydramnios 3 primary mechanisms - intrauterine anaemia - intrauteirne heart failure - hypoproteinaemia Poor prognosis, if born with hydrops 50% mortality Worse prognosis if chromosomal abnormality, cardiac anomaly (100%), other structural anoamlies apart from chylothorax, GA <24/40

Answer 203

90% non-immune 10% immune C- chromosomal - Turners, T13, 18, 21, tuberous sclerosis, noonans A - anaemia - FMH, rhesus isoimmunisation, parvovirus, alpha thalassaemia, G6PD, TAPS U - unexplained - metabolic S - Structural - Chest: CCAM, CDHB, chylothorax, hydrothorax, masses / skeletal dyplasia / GI and GU anomalies / Placental or fetal tumours T - Twins - TTTS / TAPS I - Infection - Parvovrius, coxsackie, adenovirus, STORCH (syphilis, toxo, others incl HIV, Zika, Rubella, CMV, HSV, Varicella C - Cardiac - tachyarryhtmia, bradyarryhtmia, high output state, cardiac structural anomaly - 1/3 of NIH

Answer 204

``` Previous abruption - 4% risk if one previous abruption - 25% risk if 2 previous PET Polyhydramnios Multiparty AMA Bleeding first trimester Subchorionic haematoma first trimester IVF Non vertex presentations Low BMI Premature ROM abdo trauma Smoking and cocaine Thrombophilias ```

Answer 205

``` Previous placenta praevia OR 9 Previous CS (background rate of 1%) - 1 = OR2 - 2 = OR4 - 3 : OR 22.4 Previous TOP Multiple pregnancy AMA Assisted conception Deficient endometrium: endometritis, MROP, curretage, submucous fibroid, uterine scar multiparity Smoker ```

Answer 206

SGA / FGR oligohydramnios OR 6.2 PROM OR 3.5 PTL / CS OR 4 Recommend serial growth USS and referral to clinic

Answer 207

FFP: fresh frozen plasma: coagulation factors apart from platelets. Contains fibrinogen, albumin, protein C, protein S, antithrombin tissue factor pathway inhibitor Cryoprecipitate: frozen blood product prepared from plasma. Contains fibrinogen, factor VIII, factor XIII, vWF and fibronectin GIVE - 4U FFP for every 6U of RBC or if APTT 1.5 control - platelets if plt count <50 cryoprecipitate if fibrinogen is <1g/L ``` Goals - Hb >80 Plt >75 PT <1.5 APPT <1.5 fibrinogen >1 ```

Answer 208

1:200 - increasing possibly because of CS rate and ART TVUSS 93% PPV, 97.6% NPV 90% of LLP will hav resolution by term cervical length screening can be done to estimate risk of preterm delivery and bleeding at EMCS More bleeds = more likely to have EMCS 3 or more APH OR 2.53 Management - Steroids at 34 - 35+6/40 routinely and prior to 34 weeks in cases of higher risk of preterm birth - No good evidence re outpatient vs inpatient monitoring: multiple APH likely inpatient better. OR of requiring EMCS much higher - timing of delivery - 34 - 36+6 if vaginal bleeding or risk factors for PTB - 36 - 37 if uncomplicated placenta praevia - Risks of bleeding associated with placenta praevia - 5% 35/40, 15% 36/40, 30% 37/40, 60% 38/40 - Cross match blood. RR of PPH is 4. Higher is pre op anaemia, MgSO4 use, diabetes, thrombocytopaenia. - Weekly G+H - Regional anaesthesia - Consider vertical skin and / or uteirne incision when fetus is transverse lie to avoid the placenta, particularly <28/40

Answer 209

Accreta: to endometrium basalis Increta: through endometrium basalis into myometrium percreta: through into serosa, sometimes into surrounding pelvic organs Mortality 7% in 1990s, now less 1/3 to 2/3 of cases not diagnosed pre delivery Risks - Previous accreta 4% no CS, 50-67% 3 or more CS - Previous CS delivery RR 7 first CS 0.24%, second 0.31%, third 0.6&, fourth 2%, fifth 2.3%, sixth 7% other uterine surgery repeated endometrial curretage placenta praevia - huge increases with each CS. 1 = 3%, 2 = 11%, 3 = 40%, 4 = 61%, 5 = 67% Maternal age ART MROP PP endometritis myomectomy bicronuate uterus, submucous fibroids, adenomyosis

Answer 210

``` Loss of clear zone abnormal placental lacunae - most common. With large feeding vessels bladder wall interuption myometrial thinning placental bulge - deviation of uterine serosa away from expected plane focal exophytic mass Uterovesical hypervascularity Subplacental hypervascularity Bridging vessels ```

Answer 211

no other risk factors for PTB 35 - 36+6 Slightly earlier if think major blood loss suspected Approach - CS hysterectomy - If extent of placenta accreta is limited in depth and surface area and the entire placental implantation area is accesible - can do uterus preserving surgery, including partial myometrial resection. This results in secondary hysteretomy in 30% and 4% deaths. 77% had a further pregnancy Insufficient data to recommend ureteric stents routinely Four approaches 1. Primary hysterectomy following delivery of fetus without attempting placental separation 2. Delivery of fetus, avoiding placenta, with repair of incision leaving the placenta in situ 3, Delivery of fetus without disturbing the placenta, followed by partial excision of uterine wall and repair of uterus 4. Delivery of fetus without disturbing the placenta and leaving it in sity, followed by secondary hysterectomy 3-7 days later if percreta into bladder: ureteric stents recommended. DONT GIVE ECBOLIC

Answer 212

``` Risks - 58% will need a hysterectomy haemorrhage infections and sepsis and peritonitis necrosis fistula injury to adjacent structures pulmonary oedema acute renal failure DVt PE DIC ``` RANZCOG: 2/3 will avoid hysterectomy. 17-29% recurrence of PAS.

Answer 213

Type 1: associated with velamentous cord insertion. Velamentous cord: umbilical cord inserts into fetal membranes coursing through membranes to the placenta (between amnion and chorion). No Wharton's jelly. Risk of rupture. Type 2: vessel connects the placenta with a succenturiate lobe or accessory lobe USS definition: vessel running in the free placental membranes within 2cm of the cervix If ruptures fetal mortality is 60% despite urgent CS 1/1200 - 5000 pregnancies Total blood of fetus is 80mL/kg Survival rates 97% if diagnosed antenatally and 44% if diagnosed during delivery <2cm from internal os Resolves in 20% of cases diagnosed in second trimester Repeat scan at 32/30

Answer 214

Cord inserting within 20mm of placental edge - 7% of pregnancies 25% of twin pregnancies (MC more likely)

Answer 215

Admission from 30-32/40 (particularly if high risk factors: multiple pregnancy, antenatal bleeding, TPTL) Data on TVUSS cervical measurements is limited and role of cervical cerclage is unknown Delivery: 34-36/40 ELCS Steroids 32/40

Answer 216

3% of pregnancies, associated with 40% of PTB Causes of death: prematurity, Sepsis, pulmonary hypoplasia, cord prolapse, abruption Median latency 7/7 to delivery Observe for signs of clincial chorio don't do weekly swabs (25% FP) Repeat WCC and CRP - WCC will raise 24h post steroid and should be back to normal within 3/7 (twice weekly as OP) Fetal tachycardia predicts 20-40% of chorio, FP rate of 3% Erythromycin ethylsuccinate: 400mg QID 10/7. Evidence in cochrane: chorio RR .66, babies born in 48h RR 0.7, babies born within 7/7 RR .8, neonatal infection, surfactant use, oxygen therapy and abnormal cerebral USS reduced. No difference in perinatal mortality. USe penicillin if allergy to erythromycin Corticosteroids from 24 to 35+6. Meta-analysis: RDS RR 0.8, IVH RR 0.49, no difference in NE, neonatal sepsis, apgar scores. Tocolysis not recommended - not shown to improve outcomes in cochrane. may worsen outcomes MgSO4 if <30/40 NICU invovlement OP care vs IP - cohort studies no difference Popular to offer weekly AFI and dopplers and growth every two weeks: RCTs don't show any evidence for this Emotional support: PTSD more common in women whose pregnancies are complicated by PPROM Offer IOL at 37/40 (Cochrane review of >3600 women compared planned vs expectant delivery - no difference in neonatal sepsis or infection, increased rates of RDS and CS in planned delivery pre 37. no difference in overall mrotality. No role for amniocentesis Amnioinfusion not recommendedyet but is associated with improve fetal artery pH at delivery, death, sepsis, pulmonary hypoplasia and sepsis. Cochrane If GBS positive offer IOL from 34/40. See in preterm clinic next pregnancy (RR 0.8 PPROM in next pregnancy)

Answer 217

Lancet 2001 Kenyon et al Analysing broad spectrum antibiotic use for women with PPROM <37/40 4800 women Randomised to erythromycin + placebo vs erythromycin + augmentin vs Augmentin + placebo vs placebo x 2 Primary outcome - Composite of neonatal death or severe neonatal disease (respiratory or cerebral) Secondary outcome: lots. Such as number delivered in 48h, number delivered in 7/7, RDS, NEC, birth weight, days in hospital, surfactant use, oxygen use etc. etc. Results Both Augmentin and Erythromycin decreased the primary outcome but wasn't SS Both Augmentin and Erythromycin significantly decreased number birthed within 48h, and 7/7 Augmentin 4 x risk of NEC Both decreased chorio, neonatal infection, surfactant use, O2 use, cerebral USS abnormal results Impression - Erythromycin decreases composite primary outcome and prolongs gestation - Avoid Augmentin - NEC x 4 fold. Limitations - No data collected on past obstetric history, other fetal or maternal disease Earliest gestaion not specified uncertain long term imapcts Strengths - LArge multicentre RCT blinded trial Not many lost to FU Erythromycin cheap and widely available

Answer 218

Lancet 2008 Kenyon et al 7y FU from ORACLE trial to assess any long term benefit or adverse outcomes 75% response rate, retrospective cohort trial Primary outcome: presence of functional impairment from a validated questionaire. Asked questions concerning hospital admissions, respiratory symptoms, neurobehavioural questions, medical conditions, convulsions No change in primary outcome for any of the groups No difference in death, neurobehavioural outcomes, CNS / developmental issues, diabetes, bowel issues Strengths - Large cohort - Good response rate - Validated standardised quesitonairre used No difference in response rate between groups Limitations - Recall questionaire from parents. Relies on parents understanding of childrens medical conditions - Under-represented were those from lower socioeconomic class

Answer 219

Lancet 2016 Morris RCT, blinded to assessors, ITT 1800 women 9 year study period Included if PPROM 34-36+6 (included into study if ROM prior to 34/40 and made it to 34/40_ Randomised 1:1 to immediate management vs expectant and IOL after 37-38/40 Primary outcome: neonatal sepsis: no difference Secondary outcome - Neonatal morbidity: increased RDS in immediate, increased NICU stay in immediate, increased CS in immediate - Maternal morbidity. Decreased fever in immediate, decreased hospital stay in immediate Interpretation: expectant better to reduce prematurity complications Limitation: 9 yr study design, women not blinded, hospital polices differed Strengths: RCT, multi centre, assessors blinded

Answer 220

1. Cervical incompetence 2. Decidual haemorrhage e.g. abruption, uterine overdistension such as poly or multiples 3. Uterine distortion e.g. mullerian abnormalities, fibroid uterus 4. Cervical inflammation e.g. BV, trich etc 5. Maternal inflammation / fever e.g. UTI 6. Hormonal changes - maternal or fetal stress mediates this 7. Uteroplacental insufficiency e.g. HTN, IDDM, drug abuse, smoking, alcohol consumption 8. Genetic predisposition 3 genes associated with PTB 9. Fetus recognizes a hostile environmental and activates the fetal-placental parturition pathway Microbial induces intra-amniotic inflammation, decidual haemorrhage or vascular disease, decidual senescence secondary to poor implanation, disruption of maternal fetal tolerance with allograft rejection, decline in progesterone action, etc

Answer 221

Extracellular matrix glycoprotein that sits between chorion and decidua - glue that holds pregnancy to uterus. Present in very low levels in cervicovaginal secretions >22/40, <50ng/mL. Very high levels in amniotic fluid. - NPV = 99.5% - Sensitivity 56% - Specificity 84%

Answer 222

30mm 10th centile RR 3.8 27mm 5th centile RR 5.4 22mm 2.5th centile RR 6 ``` >25mm = 1% <15mm = 4% <5mm = 78% ```

Answer 223

RR 0.74 if short cervix RR 0.64 if short cervix and previous PTB RR 0.57 in those with short cervix and midtrimester loss Offer if - ≥3 previous PTB <33+6/40 and / or second trimester losses - USS indicated: women with one or more spontaneous PTB (<33+6) or second trimester loss AND cervical length ≤25mm before 24/40 Risks - Uterine contractions, bleeding, infection, miscarraige, preterm labour, CS

Answer 224

Decreases oxytocin receptors Decreases sensitivity to oxytocin Increases prostaglandin dehydrogenase which decreases prostaglandins Decreases repsonse to prolabour genes such as connexin 43

Answer 225

Luteal phase progesterone supplementation to promote fertility and prevent miscarriage: heterogeneity in evidence Unselected population: no evidence Threatened miscarriage: preliminary evidence RR 0.53 Unexplained recurrent miscarriage: PROMISE trial no difference Assisted reproductive techniques: yes Asymptomatic short cervix <25mm in mid trimester: yes Previous PTB: consider

Answer 226

RCT, placebo controlled, double blinded Tertiary medical centre in Brazil, high rate of PTB High risk singletons included if at least one spontaneous PTB, previous prophylactic cerclage and therefore inferred incompetent cervix, uterine malformation 100mg PV suppository between 24-34/40 Swabs at entry and UA monitoring each week ONLY 157 women Primary outcome: PTB <37/40 or PTL Half the rate of PTB - significant Tocolysis worked better for progesterone group by >twice - delayed PTB rate <37/40 Small sample size Very high preterm birth rate Women had extensive follow up Women had vaginal infections treated

Answer 227

NEJM 2007 Multicentre, double blinded, RCT Aim: does progesterone pessaries reduce risk of PTB pre 34/40 in asymptomatic women with demonstrated cervical shortening on mid-trimester screening Singleton or twin pregnancies, with routine anatomy scan TVUSS cervical screening showing length <15mm Exclusions: major fetal anomaly, painful contractions, SROM, cerclage Progesterone PV vs placebo 24 - 33+6 Outcome spontaneous PTB <34/40 Secondary outcomes: neontal morbidity and LBW Screened 25,000 women and entered 250 women Outcome: OR 0.56 of PTB <34/40, significant Progesterone protective against neonatal morbidiyt but not statistically significant no significant difference in twins but only 26 pregnancies included Limitations: no comment on IOL if SROM, insufficiently powered to detect secondary outcomes, relies on USS assessment Strengths: blinded, RCT, no loss to follow up, good treatemnt adherence

Answer 228

Progesterone pessaries do not reduced RDS or other respiratory complications in women with a history of previous PTB 787 women

Answer 229

Obstetrics and gynaecology magazine RCTs comparing progesterone use vs placebo for women with a singleton pregnancy and a mid trimester cervical length <25mm Primary outcome: PTB <34/40 or fetal death 5 trials RR 0.66 RANZCOG quotes this study in their cervical length guideline. says progesterone decreases delivery pre 34 weeks and fetal death by 34% No significant difference in neurodevelopmental outcomes at 2 years of age

Answer 230

Progesterone for asymptomatic women with cervix <25mm and consider progesteorne if singeltone pregnancy and history of PTB

Answer 231

Lancet 2016 Does progesterone effect long term neurodevelopmental outcomes for children at 2 years. Double blinded, multicentre RCT, placebo controlled progesteorne 200mg daily from 22 - 34/40 Recruited if previous spontaneous PTB <34/40, cervical length <25mm, positive FFN and risk factor Primary outcomes - Fetal death or birth pre 34/40, death, brain injury, standardized cognitive score at 2 y OR was in direction of benefit but wasn't significant for any of the outcomes No differences in safety or long term harm

Answer 232

Meta-analysis of individual participant data from RCTs - evaluating progestogens for preventing ptb Systematic review of RCTs comparing vaginal progesterone, IM progesterone or oral progesterone with control or with each other in asymptomatic women at risk of PTB Outcomes evaluated were PTB, early PTB, midtrimester birth, Adverse neonatal sequelae 31 trials Vaginal progesterone and IM progesterone both reduced birth before 34 weeks in high risk singeltons Absolute risk reduction greater in women with a short cervix Oral progesterone. insufficient evidence to support its use

Answer 233

MOA: alters axis of cervical canal and displaces the weight from the uterus away from the cervix. Obstructs the cervical os and protects from ascending infection Goya et al, lancet 2012. <25mm cx RCT. PTV <34/40 OR .18 Nicolaides 2016 NEJM. No difference.

Answer 234

PTB: Not cerclage unless ≥2 (≥3 at CDHB), offer surveillance, No to progesterone Short cervix, no hx PTB: progesterone, no cerclage unless VERY short Short cervix, hx PTB: Cerclage especially if cx <15mm, maybe for progesterone Asymptomatic cervical dilation: cerclage. no progesterone

Answer 235

Challenging Recommend universal TAUSS for screening of cervical length and if <35mm for TVUSS or for those whose cervix cannot be clearly seen 7% of pregnancies in Australia and NZ occur pre 37/40, 3% pre 34/40 70% of total perinatal mortality from this 2/3 of women have no risk factors TAUSS with full bladder, use cut off of >35mm because often overestimate length. this has a 96% sensitivity for detecting cx length of 25mm. Specificity low 10th centile = 30mm = RR 4 5th centile = 27mm = RR 5 2.5th centile = 22mm = RR 6 Published data for cost effectiveness in NZ and Australia is lacking but several US studies have shown to be a small increase in overall medical costs Australia has implemented this universal screening NZ has not yet offered it - progesterone funded for cervical length <25mm and hx of PTB ≤28/40 CIN is an independent risk factor - Cone: RR 4.5 <28/40, 3 <32/40, 2.7 <37 - LLETZ RR 3 <28/40, RR 2 <32/40, RR 1.5 <37/40

Answer 236

Reduces perinatal death , neonatal death, RDS, IVH, developmental delay. No effect on BW No difference in maternal outcomes (GIVE <34+6)

Answer 237

Hyaline membrane disease Prematurity = surfactant deficiency and structurally immature lung. This results in atelectasis, which results in V/Q mismatch, hypoxia, hypercapnia, hypoventilation. This results in a respiratory acidosis and hypoperfusion which results in a metabolic acidosis. this results in further reduced surfactant production. Also pulmonary vasoconstriction which increases R heart pressure, pushes r -->L shunt of blood through FO and DA. Pulmonary vasconstriction as well as barotrauma and high fraction of inspired ocygen also results in capillary leakage, inflammation of alveoli, further decreasing surfactant production and inactivating surfactant from plasma inhibitors. Proteinaceous exudate ++ in alveoli = RDS. Lung injury = chronic lung disease

Answer 238

Lancet 2006 RCT Use of repeated doses of corticosteroids for women at risk of PTB, and neonatal outcomes NZ and Australia Crowther et al 1000 women Placebo or steroids Women who had received 2 doses of corticosteroids >7/7 prior and are still at risk of PTB, without any contraindication Rescue dose given weekly until 32/40 or birth if considered still at risk Primary outcomes: RDS, intubation, oxygen use, weight at hospital discahrge Secondary outcomes: chorio, neonatal morbidity Reduction in RDS Reduction in severe lung disease and no lung disease No other differences Safe to give - no short term harm (FU 2y: NEJM 2007, crowther et al. possible difference in attention problems, otherwise nill differences between groups

Answer 239

2016 NEJM Gyami-bannerman et al Aim: assess whether steroids should be given to women who are at risk of late preterm birth to reduce neonatal morbidity 2800 women RCT, blinded, placebo controlled Steroids x 2 doses, vs placebo Inclusion crtieria: 34 - 36+5, high risk of preterm birth e.g. contracting, 3cm dilated or 75% effaced and membranes intact, or SROM etc Excluded if imminent delivery, already had steroids, chorio, non reassuring fetal status Primary outcome: need for respiratory within 72h or death Secondary outcome: lots. Basically any kind of neonatal or maternal morbidity Primary outcome OR 0.8. Significantly less respiratory compromise Secondary outcomes: only one which was significant was neonatal hypoglycaemia RR 1.6 Limitations: significant number of woman only got one dose No tocolysis No documentation of neonatal hypoglycaemia numbers over time BEnefits Large multicentre RCT, blinded, placebo controlled Consistent with ASTECs

Answer 240

2005 BMJ Multicentre, RCT, placebo controlled Incidence of RDS is much higher in CS vs NVB (3.6% vs 0.5%) Steroids vs no steroids pre term ELCS Primary outcome: SCBU admission for respiratory support . RR 0.46 Secondary outcome: level of respiratory disease - Incidence at all of RDS 0.21 RR - TTN o.54 RR

Answer 241

CCB RR 0.3 birth within 48h Decreased RDS, IVH, jaundice, NIcu admission, NEC Don't give if - >34/40 - CHF, MI, angina - singificant bleeding or abruption - Fetal anomaly not consistent with life - Maternal indication for delivery - Fetal distress

Answer 242

<30/40 4g loading dose then 1g/hour maintenance dose until birth or 24h ``` Monitor RR HR Reflexes UO BP ``` Stop if RR <12, absent patellar reflexes, UO <100mL/4h, hypotension Give 1g calcium gluconate if concerned about toxicity

Answer 243

A disorder of movement or posture or both, and a disorder of motor function which is permanent but may change over time. Happens at any time of brain development 2/1000 live births Most frequent cause of major motor disability 42% of cases associated with preterm birth ``` Biggest risk factors - Very preterm birth <34/40 - Very low birth weight <1500g Twins 7x risk Triplets 47 x risk IVH ```

Answer 244

Essential 1. Evidence of metabolic acidosis with a pH <7 or BE <12 in cord arterial sample or early neonatal sample 2. CP of the spastic or dyskinetic type 3. Early onset of neonatal encephalopathy in infants ≥34/40 Suggestive 1. An acute, severe and sustained change in fetal heart rate pattern when it was previously normal 2. A sentinel hypoxic event in labour 3. An apgar score of ≤6 at 5 minutes 4. Early evidence of multisystem invovlement 5. Early evidence of cerebral abnormality on imaging

Answer 245

2009 cochrane review Involved 5 RCTs that looked at MgSO4 vs placebo for neuroprotection or tocolysis or PET - Included MagPIE study - Included Crowther et al NZ study Proven to decrease CP rates - RR 0.68 No change in any other neonatal morbidity or mortality NNT = 63 Limitations: large variety within the studies Benefits: large number

Answer 246

25% no active treatment 1/10 die during resuscitation 65% make it to NICU - 50% of these will make it home - 20% of survivors will have major neurodevelopmental issues / CP (6%) - 10% of survivors will have less major neurodevelopmentla issues / CP (3% overall) - 60% of survivors will have mild neurodevelopmental issues or be fine (18% overall)

Answer 247

``` 6% no active treatment 2% die in resus 92% make it to NICU - 64% will make it home - 70% of survivors mild disability ```

Answer 248

``` Recognise Communicate Resuscitation Monitor Investigate Directed Treatment ```

Answer 249

500 - 1000. Normal BP. Slightly tachycardic. Lightheaded. Palpitations. 1000-1500. Slightly low BP. HR 100-120. Weak, diaphoretic 1500 - 2000. SBP 70 - 80. HR 120-140. Confused. Restess. Oliguria 2000 - 3000. SBP <70. HR >140. Collapse. Air hunger, Lethargic.

Answer 250

1:1200 - 8000 | 15% mortality

Answer 251

1. Johnson's Manouvre - Replace uterus with hand, aiming for umbilicus - STOP UTEROTONICS 2. Hydrostatic technique - close off vagina with siolastic cup or neonatal mask or foleys balloon and fill vagina and uterus with warmed saline. Need 2 - 4 L usually. 3. Laparotomy - Hungtingtons technique: use atraumatic grasper such Allis or Babcock to pull up the Round ligament, placing the clamp more medial each time more of it is seen. Can replace vaginally at same time. - Haultain's technique: cut cervical ring stricture posteriorly to allow more space to replace uterus with Hungtington's procedure

Answer 252

Direct - HAemorrhage - VTE - Hypertension Indirect - CVD - Suicide - Haemorrhage from a non-obstetric source such as splenic artery rupture, ICH

Answer 253

Haemorrhage Hypoxia Hypo or hyperkalameia and hyponatraemia Hypothermia Toxins Tension pneumothorax Tamponade Thromboembolism +eclampsia

Answer 254

6/100,000 Says leading direct cause of maternal death in Aus and NZ 15% mortality rate, used to be 80% Triad: acute hypotension, hypoxia, coagulopathy 1. Pulmonary vascular occlusion, vasoconstriction --> pulmonary hypertension. RHF, pulmonary oedema, LHF, cardiac arrest 2. Anaphylactoid type response, vasodilation and third spacing, acute hypotension 3. Plasminogen activator causing fibrinolysis and procagulants released causing consumptive coagulopathy --> DIC

Answer 255

``` Skin Subcutaneous tissue Supraspinous ligament Interspinous ligament Ligamentous flavum Epidural space Dura Intrathecal space CSF ```

Answer 256

Symptoms: first feel inebriated, disorientated, lightheaded, circumoral anaesthesia, twitching, loss of consciousness, respiratory or cardiac arrest, convulsions, bradycardia Pathogenesis: local anaesthetic blocks sodium channels in the heart and slows conduction leading to bradycardia and eventually heart stops. Treatment Stop epidural ABC 20% Intralipid 1.5mL/kg bolus over 1 minute then 15mL/kg/hour infusion Can give up to 2 more boluses if required

Answer 257

1-3/100,000 1% mortality Respiratory: bronchospasm, mucous plugging, airway oedema, hypoxia Skin: urticaria, rash, flushing Cardiac: rapid depletion of intravascular volume --> decreased CO --> cardiac arrest Treatment 0.5mL 1:1000 Adrenaline IM Repeat after 5 minutes if no improvement Also antihistamine: chlorpenamine and 200mg IV or IM hydrocortisone

Answer 258

Increased - Plasma volume by 50%, red cell mass by 30%: dilutional anaemia, less oxygen carrying capacity - CO increased by 30%, 80% in labour, 100% PP. More circulation demands during CPR - HR increases by 20bpm - Hypercoagulable: susceptible to thromboembolism - Levorotation of heart: ECG changes. More difficult to interpret - Oestrogen increases myocardial excitability: more SVT Decreased - SVR: sequesters blood - systemic return when supine: sequesters blood, need L lateral tilt - BP: more at risk of MI - Pulmonary pressures: increased risk pulmonary oedema

Answer 259

Increased oxygen consumption and metabolic demand: hypoxia occurs sooner Metabolic alkalosis secondary to increased RR and decreased CO2. Decreased buffering capacity Laryngeal oedema: more difficult intubation Decreased funtional residual capacity which decreases buffering capcity Decreased bicarbonate in blood - decreased buffering capacity

Answer 260

Decreased gastric motility, lower oesphageal pressure - increased risk of aspiration

Answer 261

750mL/min blood flow to uterus, potential to lose a lot of blood quickly. Sequesters blood in CPR No autoregulation of uterine vessels, uterine flow decreases ++ with drop in blood pressure Fetus has 2 minutes of oxygen available to them in a maternal apnoea Cannulate above diaprhagm PERIMORTEM CS after 20/40 if no response to CPR after 4 minutes

Answer 262

Breast hypertrophy = hard to do compressions WEight on chest Increased compression force required and slightly higher becasue of left heart displacement

Answer 263

First stage - Spinal pathways (parasympathetic and sympathetic), T10-L1 - visceral sensation. Crampy. - Mechanical receptors (pressure) and chemoreceptors (bradykinin, histamine, serotonin, acetylcholine release from myofascial injury). Referred upper abdomen and back. - Inferior hypogastric plexus S2-4 pressure on bladder / rectum (referred to sacrum / perineal area) Second stage - Somatic nerves - S2,3,4 pudendal nerve - Ilioinguinal nerve (L1) - Posterior cutaneous nerve of thigh (S2-3) - Genital branch of genitofemoral nerve (L1-2)

Answer 264

What works: epidural, CSE, inhaled analgesia What may work: water immersion, acupuncture, massage, relaxation, LA nerve blocks, non-opioid drugs Insufficient evidence: IV opioids, hypnosis, biofeedback, TENS, sterile water injections, aromatherapy

Answer 265

Indications - FTP - Cervical oedema - Patient request - Increased risk of instrumental birth - Twins Contraindications -Maternal refusal Relative contraindications - On anticoagulants - Plt <80 - Skin infection - Generalised sepsis - Hypotension - CVS instability - Unable to cooperate - Stenotic heart lesions - Abnormal spinal anatomy

Answer 266

Common: pain at site, bruise at site, (used to be increased risk of instrumental - now not true), 5% technical difficulties (doesn't work or unilateral) Uncommon: fetal distress, Post dural puncture headache (1/200), hypotension, pruritis, N+V Rare: <5/million risk of paralysis, <1:13000 risk of nerve damage High block (>T4 - nipples) Local anaesthetic toxicity

Answer 267

Lancet 2000 Hannah et al Multicentre, international, RCT CS vs planned vaginal breech Inclusion: singleton, breech, >37/40 Exclusion: footling breech, EFW >4000g, palpated LGA, hyperextended head, other reason for CS, fetal anomaly not compatible with NVB, lethal fetal anomaly Primary outcome: perinatal mortality or serious neonatal morbidity Secondary outcome: serious maternal morbidity or maternal mortality Results 2000 women, 121 centres ITT Primary outcome RR 0.33 - significant. 5% vs 1.6% Perinatal mortality: 0.3% CS, 1.3% NVB RR 0.23 Serious perinatal morbidity 1.4% CS, 3.6% NVB RR 0.36 No difference in secondary outcomes Limitations: Didn't adhere to inclusion / exclusion criteria very well. Lots of deaths included were not secondary to a vagina Differences in low perinatal mortality countries much much higher than in developing countries.

Answer 268

Breech 3-4% at term Risks - EMCS 1/200 - abruption, fetal distress, cord prolapse - Transient fetal distress 0.37% - ROM - APH 0.5% - Fetal death 0.019% Absolute contraindications - CS needed regardless - APH last 7/7 - Fetal anomaly not consistent with NVB - Abnormal CTG - ROM - Rhesus isoimmunisation - Multiple pregnancy Relative contraindications - SGA with abnormal dopplers - Oligohydramnios - Uterine anomaly - ??Previous CS - controversial as one study shows no greater risk in comparison to someone without a scar on uterus - PET - Major fetal anomaly

Answer 269

0.1 - 0.6% 1% breech 1% mortality

Answer 270

Normally aerobic metabolism occurs. Glucose --> pyruvate in presence of oxygen then gets converted to CO2 and H2O and makes 36-38 ATP molecules Anaerobic metabolism. Mobilises glycogen stores, converts to pyruvate, in absence of oxygen converted then to lactic acid and 2-3 molecules of ATP. Lactic acid slowly diffuses back across placenta so can build up quickly in fetus. Also, if mother has high alctic acid this also slows diffusion across placenta. FBS lactate >4.8 = pH <7.2, urgent delivery required FBS lactate 4.1 - 4.8 = pH 7.2 - 7.24, repeat in 30 minutes

Answer 271

Apgar <4 at 1 minute Apgar <7 at 5 minutes Operative delivery for fetal distress FBS performed in labour Proven to decrease acidosis (provides feedback about CTG interpretation) Very different values accepted compared to FBS as lactic acid accumulates in labour. Arterial values can be normal up to 7.5 The arterial sample should be a minimum of 0.6 above venous sample

Answer 272

1st and 2nd wave of trophoblast invasion abnormal Spiral arteries don't develop into low resistance, high capactience vessels This results in increased PI of uterine arteries and bilateral notching Useful to differentiate a SGA vs FGR fetus

Answer 273

Decreased intervillous oxygen supply (often secondary to abnormal spiral artery development) leads to decreased oxygen delivery to the fetal side of the placenta and persistent vasoconstriction of the stem villi. This increases the resistance through the umbilical arteries. Increased resistance is associated with fetal hypoxia, acidosis and increased perinatal mortality and morbidity. UAPI is used to time delivery after 32/40 - Deliver by 32/40 if reversed end diastolic flow - Deliver by 34/40 if absent end diastolic flow - Deliver by 38/40 if raised UAPI with positive end diastolic flow

Answer 274

Middle cerebral artery PI is measured in the circle of willis. When the fetus is in a state of hypoxia, it vasodilates the MCA to enhance perfusion to the brain. This is shown as a low resistance in the MCA PI. It is not directly associated with acidosis because fetuses may compensate for weeks before becoming acidaemic and unwell but is related to increased risk of CS (50%) and fetal distress in labour. - FGR and abnormal MCA – deliver by 38/40

Answer 275

This is a measure of resistance in the ductus venosus which shunts blood from the umbilical vein to the IVC. Increased amount of blood is shunted through this in the context of hypoxia. As the fetuses heart works harder in a hypoxic environment preload and afterload increase, right heart pressures increase, so pressure increases in the ductus venosus. It begins as an increased resistance (PI) and then results in absent a wave (atrial contraction) and then reversed a wave It has a moderate predictive value for acidaemia and adverse outcome. Prospective studies show that ductus venosus flow is the best cardiovascular parameter in the prediction of acidaemia at birth and adverse perinatal outcomes in severe early onset FGR

Answer 276

Variable decels = cord compression Compression of vein first as thinner wall. Slow decrease in RH pressure and oxygen, means sympathetic input increases and FH increases to try and get more oxygen = Pre- shoulder. Then artery gets compressed, sudden increase in pressure, decrease in Oxygen. Chemoreflex = parasympathetic input = decreased FH to try and decreased myocardial workload and protect heart from iscahemic insult = drop in FH to bottom of variable decel. Then artery is no longer compressed, so low FH with low oxygen, low CO and low blood pressure, so parasympathetic input is taken away so FH starts to rise again. Venous output is still compressed so sympathetic input increased to try and get more oxygen from placenta - get shoulder.

Answer 277

Chronic hypoxia in intervillous space. Fetus doesnt have enough oxygen to respond appropriately to cord compression / contractions - Late decelerations are: o Uniform in timing relative to contraction o Repetitive in nature o Will occur with each contraction Start after contraction starts and nadir is 20 seconds after peak of contraction

Answer 278

``` Hb <50 2-5 cycles per minute 5-15bpm above and below baseline smooth oscilating pattern Reflects a complete loss of autonomic control ```

Answer 279

Heart rate is controlled primarily by the sinoatrial node in the R atrium, which has parasympathetic (Ach and vagus) and sympathetic input (adrenaline + noradrenaline). Adrenal glands produce adrenaline (80%) and noradrenaline (20%) which are the major catecholamines (with dopamine) that act on FHR, causing peripheral vasoconstriction, increased BP and redirection of O2 to brain, heart and adrenals. Chemoreceptors: high metabolic rate requires high O2 demands, therefore very sensitive to decreased oxygen saturations in blood. Located in aortic arch, carotid and brain stem. - Gradual ↓O2 causes chemoreceptors to signal the cardiac regulatory centre (CRC) to increase sympathetic nervous system activity on SA and ↑ heart rate - Abrupt ↓ in O2 causes chemoreceptors to stimulate parasympathetic activity via the vagus nerve and Ach, causing ↓ FHR Baroreceptors act to protect the brain from extremes in blood pressure by acting on the parasympathetic system. - Hypotension causes them to signal CRC vagus withdrawal and ↑ HR - Hypertension causes increased vagus nerve stimulation and ↓ FHR Cardiac regulatory centre in medulla oblongata of brain stem co-ordinates and regulates response to O2 saturations.

Answer 280

Suboccipitalbregmatic - OA: 9,5cm occipitofrontal: deflexed OP 11.5cm Mentovertical: brow: 13.5cm submentobregmatic 9.5cm

Answer 281

``` <34/40 Uncertain of position Bleeding disorders or thrombocytopenia Osteogenesis imperfecta Face presentation ``` Relative - 34-36/40 - Prior FBS 10% rigid cup 15% soft cup

Answer 282

``` Minor scalp or facial injuries Cephalohaematoma (soft cups > hard cups > forceps) Sub galeal 1/300 shoudler dystocia Facial nerve palsy Corneal abrasion Retinal haemorrhage Skull fracture or intracranial haemorrhage - 1/600 forceps - 1/850 vacuum - 1/ 900 EMCS in labour - 1 / 1900 SVB - 1/2750 ELCS ``` Maternal risks - Vaginal trauma - OASIS - PPH - Earlier cessation of BF - Incontinence

Answer 283

Lancet 2019 1700 women, Augmentin vs placebo Primary outcome: infection wihtin 6 weeks 11% vs 19%, RR 0.58

Answer 284

0 - 2 Appearance: pale / pale peripheries only / pink Pulse: no pulse / <100 / 100-140 Grimace: no cry / weak cry when stimulated / strong cry when stimulated Activity: no tone / some flexion / flexion and reisisted extension Resp rate: apnoeic / slow irregular breathing / strong cry

Answer 285

1/300 instrumentals, mostly ventouse 0.6/1000 any delivery Bleed from emissary vessels breaking under the epicranial aponeurosis and above periosteum of skuil Potential space to bleed 250mL into - 50-70% of blood volume. 38mL = 1 extra cm of HC Gravity dependent, thrill with a flick, can displace ears and cause eyes to become very oedematous. Lesion becomes more fluctuant over time. Pitting oedema over head and in front of ears 12-25% risk of mortality if admitted to NICU Anaemia, hypotension, acidosis, pain, coagulopathy Vaccum OR 7 Forceps OR2.6 Other risks: nullip, apgar <7 at 5 mins, paramedian cup placement, cup too anterior, failed vacuum, prolonged vacuum

Answer 286

Bleed underneath the periosteum Doesn't cross suture lines Can increase over first 24h but then will stop. May take weeks to disappear

Answer 287

1. Increased age to 25 2. REcommend examination if symptomatic 3. If >70 and hasn't been screened or inadequate screening lasgt few years, for 2 screening tests 1 year apart 4. If treat HrHPV for 6 and 12 month FU with cytology and HrHPV test

Answer 288

HPV types 6, 11, 16, 18, 45, 31, 33, 52, 58 97% efficacy Gardasil 4: 6, 11, 16, 18 50% reduction in SCC Vaccine: contains virus like proteins only

Answer 289

1. International consenus, many european countries start at 25 or 30 2. Englands implementation didn't increase incidence in 20-25yo 3. Australias implementation didn't increase incidence in 20-25y 4. Leads to overtreatment and secondary harm such as anxiety, harm from treatment 5. harms outweigh benefits: 15% PTB LLETZ and 7% general population 6. Low evidence of cervical cancer incidence and mortality in NZ in 20-25yo 7. HPV vaccine introduction has decreased colposcopy abnormalities which has resulted in deskilling - lower sensitivity and lower PPV 8. HIGH chance of regression in 20-24yo

Answer 290

3-5% coagulates the nuclear proteins and shows up white Higher the nuclear activity = more white Some inflammatory lesions All CIN Rapidity of colour change also significant

Answer 291

Afferent and efferent vessels get compressed during normal metaplastic process. During diseas and dysplasia these vessels get incorporated and trapped between the cells. They look punctate (head on) and this is called mocasicism punctation. Coarse vessels - high grade Fine vessels - low grade Cork screw vessels, comma vessels, character writing vessels

Answer 292

CIN1 - 1% CIN2 5% CIN3 12%

Answer 293

GOOD EVIDENCE FOR 1. Prophylactic abx. Ampicillin or first generation cephalosporin - decreased endometritis by 60%, infection from ELCS by 25% and EMCS by 65%. Addition of azithormycin halves the infections further (6 vs 12%). 3g for obese women 2. Cephalad - caudal blunt extension of incision 3. Spontaneous delivery of placenta 4. Oxytocin infusion for PPH prevention 5. Single layer uterine closure for women who have no future fertility desire 6. Closure of subcutaneous layer if >2cm Other measures to consider Pre op 1. Thromboprophylaxis (no difference in rates of VTE in large retrospective cohort study AJOG) 2. Vaginal prep - Endometritis rates decreased from 9.4 to 5.2% (cochrane) 3. No urinary catheter reduces rates of UTI from 5 to 0.5%. Studies were underpowered to detect the difference in bladder injury 4. Oxygen - no benefit 5. Skin prep and hair removal: chlorhex better than iodine. Clip, don't shave hair The procedure - Joel cohen: less fever, pain, analgesic requirements, reduced blood loss, operative time and a shorter stay in hospital - No dissection off rectus muscle inferiorly = less pain - Uterine incision: blunt extension = reduced blood loss. Cephalad - caudad transverse blunt expansion rsults in less uterine incision extensions and reduction in EBL - Spontaneous placental delivery with CCT and fundal massage: lower rates of endoemtritis, less blood loss - PPH prevention: IV oxy or carbetoxin. More evidence of infusion than bolus. Miso similar but more side effects. TXA reduction in blood loss. - Cervical dilation not recommended, no difference in morbidity - Exteroirisation no difference - Single vs double layer closure - short term outcomes comparable. Case control studies suggest thinner residual myometrium if single layer - only for women with no desire for future fertility - Peritoneal closure: no good evidnece. not closing = shorter operating time etc. Possibly less abdominal adheisons if close - SC tissue: close if ≥2cm RR 0.6 of wound disruption and RR 0.42 of seroma formation - No evidence for SC drains - Skin closure: sutures better than staples, less wound separation.

Answer 294

16/100 complication in ELCS 24/100 in EMCS if labour ``` Serious risks - Emergency hysterectomy : 7-8/1000 - Further surgery required: 5/1000 - Admission to ICU: 9/1000 - Thromboembolic disease: 4-16/10,000 - Bladder injuru 1/1000 Ureteriv injury 3/10,000 Death 1/12,000 ``` Future pregnancies - Uterine rupture 2-7/1000 - antepartum stillbirth 1-4/1000 - Placenta praevia / accreta: 4-8/1000 Frequent risks - Persistent wound and abdominal discomfort in the first few months following surgery 9/100 - Requirement of a repeat CS when VBAC attempted: 1/4 Readmission to hopsital 5/1000 HAemorrhage 5/1000 Infection 6/100 Fetal laceration 1-2/100

Answer 295

Switch on pulmonary epithelial sidium channel genes that switch from lung fluid secretion to absorption and increased surfactant production And increases surfactant production RANZCOG recommends consideration given to steroids if pre 39/40

Answer 296

BMJ 2005 Stutchfield et al Aim: do steroids reduce respiratory distress in babies born y ELCS at term? (Background: incidence of RDS is 3.6 vs 0.5% in CS vs vaginal) Multicentre RCT, not blinded Primary outcome: admission to SCBU with respiratory distress Secondary: severity of RDS and level of care in response 1000 women ``` Results - Primary outcome: RR 0.46 - TTN RR 0.54 Incidence of RDS 0.21 NICU requirement 2 vs 14 ``` ``` - Strengths: o Randomised o Good effect sizes o Pragmatic – applicable to real life - Weaknesses: o Not blinded or placebo controlled ```

Answer 297

GnRH pulsatility LH release in pulses Also FSH release but usually more controlled by oestrogen and inhibin FSH release causes a primary follicle to create an early secondary follicle (granulosa cells, zona pellucida, oocyte (diploid)) LH causes cholesterol to be converted to androgens in the theca cells Then FSH causes granulosa cells to produce oestrogen from androgens (P450 aromatase) FSH causes further proliferation of granulosa cells which produce follicular fluid which are high in hyaluronic acid - late secondary follicle Pockets of fluid coalesce and form antrum to make and antral follicle. FSH then recruites one follicle to forma graffian follicle or tertiary follicle. Secondary occyte in this (underwent meiosis I). Now diploid stem cell has goen to 2 daughter cells (haploid) and one is polar body so undergoes degeneration, one is secondary oocyte.

Answer 298

Oestrogen negative feedback on GnRH and FSH and LH. Switches when reaches a certain concetration of oestradiol to positive feedback. +ve feedback ++ to GnRH which stimulates large LH surge and a smaller FSH surge Graffian follicle produces inhibin B which inhibits FSH This results in LH stimulating blood flow to granulosa cells / antrum to produce more follicular fluid rapidly Proteases then eat away at granulosa cells and cause the secondary oocyte to pop out of the graffian follicle LH then causes luteinization and helps form CL CL produces progesterone +++ HCG maintains CL for 4-5 weeks if get pregnant, otherwise involutes after 14 days

Answer 299

Proliferative (6-14) FSH --> oestrogen --> stimulates stratum functionalis to proliferate, spiral and coil arteries to increase (angiogenesis). Oestrogen causes uterine gland formation Oestrogen causes mucus to be thin in cervix so sperm can swim up through the mucus helps with capacitation Secretory (15-28) As CL is produced and produces progesterone Progesterone stimulates the spiral and coil arteries to become longer (angiogenesis) and casues thickening of the stratum functionalis. It causes the uterine glands to secrete rich fluid full of proteins, lipids and glycogen to allow for implantation Mucus becomes thicker to prevent further sperm and infection coming up Implantation occurs when more progesterone is around Menstruation (day 1 - 5) No pregnancy = no HCG = CL not maintained and progesterone drops This results in vessel spasms (progesterone maintains balance between vasoconstriction and vasodilation) and weakening of vessels. Blood rushes in and the vessels burst, blood fills the area. This results in decreased nutrients and oxygen, iscahemia and then sloughing off of the layer (Pathological length of cycle = <21/7 or >40)

Answer 300

``` GnRH --> LH and FSH Primary spermatogonia (2n) undergo mitosis, producing 2 daughter cells (2n), one daughter cells continues to replicate under mitosis, the second daughter cell is released into luminal area and undergoes meiosis. It goes from a parimary spermatocytes, under meiosis I into 2 daughter cells both haploid. Meiosis II then results in 4 daughter cells (1n). These cells are called speramtids now and develop into functional sperm. ``` LH stimulates leydig cells to produce an enzyme that converts cholesterol to testosterone FSH stimulates sertoli cells to produce androgen binding proteins that help keep a high concentration of soluble testosterone in the vicinity to continue spermatogenesis. Sertoli cells also provide nutrients to the sperm. Testosterone exerts negative feedbakc on the hypothalamus resulting in lower GnRH, LH and FSH to decrease production of testosterone. Black sensors on edge of sertoli cells detect levels of sperm cells and once they get to a certain concentration inhibin is produced which exerts a further negative feedback on hypothalamus and anterior pituitary. Spermatogenesis slows down

Answer 301

Erection controlled by PSNS (S2-4) - Innervates blood vessels in corpus cavernosum by Ach, stimulate NO production from arginine, dilate, fill with blood, pinch off venous return, erection. High PSNS input, then switches to SNS (T12 to L2, hypogastric plexus) SNS releases NE which stimulates epididymis to contract and release sperm into the vas deferens, vas deferens to contract and push sperm up through it, seminal vesicles to contract and release seminal fluid and internal urethral sphincter to contract and prevent retrograde ejaculation. Sperm moves into common ejaculatory duct and into prostatic urethra and then Bulbospongiosus also contracts (Pudendal nerve via Ach) resulting in ejaculation.

Answer 302

70% of seminal fluid released from seminal vessicle, high in fructose, coagulase and PG 30% from prostate - high in fibrolysin, citrate, relaxin, PSA Fructose - sperm to use this in their mitochondria to make ATP and they can move their flagella, swim up through vagina Coagulase is used to bind to walls of vagina. Fibrinolysin breaks down some of this coagulation Prostaglandins cause backwards contractions of uterus allowing sperm to enter uterus Uterus is a more alkaline environment which allows sperm to swim faster (over an acidic environment) Seminoplasmin is an antibiotic chemical which inhibits microbial activity in uterus Oestrogen causes cervical and endometrial glands to make fluid that helps with capacitation Capacitation is when the sperm loses proteins and cholesterol from its head so it can swim faster and get through the hyaluronic acid / granulosa cells (hypermotile) Sperm then makes it to and binds to zona pellucida which results in a release of chemicals from the sperms head which results in acrosomal reaction which is when the acrosome fuses after calcium ions run into the sperms head which results in proteases being released and helps burrow a hole in zona pellucida. Sperm makes it to the basement membrane of the oocyte and binds to the beta subunit of basement membrane. This results in a +ve charge over the basement membrane - FAST BLOCK TO POLYSPERMY The sperm then binds to alpha subunit on basement membrane and the DNA material from the sperm is released into the oocyte This causes the smooth endoplasmic reticulum to release more Ca++ and lysosome which breasks down the zona pellucida (preventing anything for th e sperm to bind to) and hardens the basement membrane which is the SLOW BLOCK TO POLYSPERMY. It also causes the oocyte to complete meiosis II and degrades the polar body. The two haploid cells become a diploid cell - zygote. CONCEPTION ``` Meiosis = PMAT x 2 Prophase Metaphase Anaphase Telophase ``` After zygote created then cleavage occurs while the zygote is moving towards uterus over the next four days. This cleavage occurs really fast as cells don't have time to grow, just break into two. Each cell has 46 chromosomes. The structure is still surrounded by the Zona pellucida. It becomes a Morula! The morula enters the uterus. Then compaction occurs inside the morula. It creates two types of cells - trophoblast around the outside and inner cell mass. It is now called a blastocyst the blastocyts implants into the secretory endomwtrium and burrows itself down into it. This happens at day 6 post conception. Trophoblast produces a proteolytic enzyme to help with this. The trophoblast divides into syncytiotrophoblast and cytotrophoblast. Day 10, completely burrowed, produces HCG, ZP breaks away Inside the blastocyst there are two cavities being created called amniotic cavity and yolk sac The inner cell mass creates a bilaminar disc (epiblast and and hypoblast) This bilaminar disc then creates a trilaminar disc (gastrulation - 3rd week) called ectoderm (skin, neural tube), mesoderm (bone, muscle, subcutaneous layers, cartilage, urogenital organs, peritoneal lingins of body cavities, pleura), endoderm - linings of organs such as gut, pancreas, thyroid, airway) Notochord then induces neurulation The ectoderm then starts forming a neural plate and neural tube. End of week 4 neural tube has been formed.

Answer 303

2 of 3 1. Polycystic ovaries: ≥20 follicles 2-9mm on USS (needs to >8 years since menarche and no CL or dominant follicle present) 2. Oligomenorrhoea (≤9 periods / year) or anovulation 3. Clinical and / or biochemical signs of hyperandrogenism - Hirsutism - Acne - Male pattern baldness - Free androgen index high (free testosterone divided by SHBG x 100). Typical values 7 - 10 in women.

Answer 304

Likely related to genetic and environmentla influences, and possibly whilst in utero Hyperinsulinaemia --> LH hypersecretion and potentiates the action of LH and IGF-1 which both upregulate the production of androgens form voary and adrenal gland. This results in testosterone and DHEA-S Hyperinsulinaemia and hyperandrogensim causes arrest of follicular development. Excessive androgens impair aromatase function which is required for oestradiol production and follocular development. AMH antagonises FSH also. Multiple small follciles are present, theca cells prominent becasue of LH secretion / action. Some oestradiol produced but not progesterone because no CL. Unopposed oestradiol speeds up GnRH pulses and results in LH >FSH rratio. LH thickens theca cells which results in testosterone and oestradiol --> gnRH pulsatility --> LH --> cycle Thickened endometrial lining Free testosterone and androstenione levels are rasied DHEA and DHEA-S are mildly raised total testosterone are sometimes raised (30% of patients) Low SHBG so free androgen index rasied. Normal or low FSH LH normal or elevated

Answer 305

CRH --> ACTH --> adrenal gland - Zona glomerulosa: mineralcorticoids (aldosterone) - Zona fascilulata: corticosteroids - Zona reticularis: gonacorticoids (androgens) (adrenal medulla - adrenaline, NA)

Answer 306

5 genes Most common deficiency is 21 hydroxylase Overproductino of anrogens becasue 21 hydroxylase is required to make cortisol and mineralcorticoids. Absent feedback to CRH from cortisol so increased ACTH and increased androgens Virilisation of females, ambiguous genitalia, salt wasting and adrenal crises - can result in death. Non classic CAH - 20-60% of normal function in 21 hydroxylase. Presents later in life. Oreseved cortisol and aldosterone production, so salt wasting and adrenal crises don't occur. Presents with precocious pubert, tall stature, advanced bone age, early epiphyseal fusion, infertility and severe acne

Answer 307

Overproduction of cortisol <50% from cushing's disease (ACTH production from pituitary adenoma), most from adrenal adenoma / carcinomas Very rare as associated with infertility Dexamethasone suppression test fails to suppress cortisol appropriately. - Supresses at low doses if cortisol production from adrenal - Supresses at high doses if cortisol production from ACTH production at pituitary - Doesn't supress if ACTH from ectopic places

Answer 308

1. IGT / diabetes - 4 fold increase 2. GDM 2 fold increase - early OGTT 3. MEtabolic syndrome (hypertension, rasied WC, raised LDL and cholesterol, rasied fasting BSL, rasied TG) - consider screening for everyone (with OGTT) 4. Emotional and QoL issues: depression and anxiety increased risk. As well as eating disorders, psychosexual dysfunction, 5. Cardiovascular risk: screen for other risks (obesity, smoking, dyslipidaemia, HTN, IGT, lack of physical activity). Regular weight monitoring. 6. OSA increased independent of BMI 7. Cancer and endometrial hyperplasia 8. Infertility

Answer 309

Letrozole ovulation IOL Take 5mg Letrozole from days 2 - 6 of period (If first day of period starts half way through the day and not sure proper period have day 1 as your first full day of period) Letrozole is an aromatase inhibitor so it prevents oestradiol being released from granulosa cells. This means FSH is produced without negative feedback, and more follicles are recruited. Also prevents ovulation) Have sex between days 7 and 14 Day 21 progesteorne to assess whether ovulated If high means ovulated --> either get pregnant or have a period. If period, start Letrozole again at day 2 If low means didn't ovulate --> take Provera 10mg for 5 days then stop and start letrozole again on day 2 Twins 5% If using GnRH for PCOS Induction of ovulation - SECOND LINE - give progesteone to induce withdrawl bleed and then add in slowly increasing doses of gonadotrophins until oestradiol > 400pmol/L (start at 50U then 75, then 112.5, then 125. Once oestradiol >400, do scan, then if follicle >13mm alternate day scans until one or two follicles >17mm when you can given HCG 5000 IU to induce ovulation. Ovarian drilling - may work IVF third line: GnRH antagonist protocol (over agonist) preferred with IVF +/- ICSI cycle

Answer 310

``` 1. Lifestyle modification has greatest evidence: 5-10% weight loss is assoicated with significant improvement in metabolic indices and restores menstruation S - specific M - measurable A - achievable R - realistic T - timely goals ``` 2. Pharmacological methods - all off license and minimal evidence - COC - use standard COCs first, not anti-androgen ones as they increase risk for VTE (Ginet - cyproterone, Yaz - drosperinone). If no resolution of symptoms such as irregular bleeding, hirsutism, acne etc after 6/12 of normal COC and sometic procedures, then can consider Ginet or Yaz - Metformin - minimal evidence. consider if need weight loss. Consider if on Letrozole to enahnce its use. Give if IGT or T2D. Trial suggests no superiority over lifestyle changes - Anti-hypertensives if high BP 3. Bariatric surgery 4. ART - Letrozole - GnRH - IVF

Answer 311

COC first line - use ones contaning drosperinone or desogestrel Metformin - minimal evidence for treatment of primary hirsutism Spironolactone - minimal evidence Comsetic procedures Eflornithine - topical application. Ketoconazole Weight loss

Answer 312

Prolactin normally stimulates mammory gland growth, and stimulates and maintains lactation ``` Galactorrhoea 90% amenorrhoea / oligomenorrhoea (stops GnRH pulsatility resulting in low LH / FSH and low oestrogen) low bone density weight gain Mood and behavioural changes Hypo-oestrogenism symtpoms: dyspareunia, lowered libido, Infertility Premenstrual syndrome headaches and visual disturbances rare acne hirsutism ```

Answer 313

Increased PRL production - PCOS - Piruitary tumours: adenomas, hypothalamic stalk interuption, hypophysisits (inflammation) Decreased PRL secretion: renal failure, hepatic insufficiency Physiological causes: pregnancy (via oestrogen) Neurogenic: chest wall injury, breast stimulation, breast feeding Hypothalamic PRL stimulation - Primary hypothyroidism (TRH stimulates increased PRL) - Adrenal insufficiency ``` Medications - Neuroleptics: haloperidol, phenothiazines - Antihypertensives: CCB, methyldopa - Psychotropic agents: TCA - Anti-ulcer drugs: H2 antagonists - Opiates All inhibit dopamine release. ```

Answer 314

Bromocriptine or cabergoline - dopamine agonists Stop in pregnancy unless absolutely required. No evidence of teratogenesis or malformations Visual field assessments if required Can't use if want to breast feed

Answer 315

Types 1. Premenstrual symptoms 2. Premenstrual disorder (affects QoL) 3. Medication induced i.e. on HRT 4. PMS without menstruation (e.g. hysterectomy) 5. Exacerbation of underlying disorder 40% experience PMS symptoms, 5-8% suffer from severe PMS 1% PMDD PMDD 1. Present in the week leading up to menses, reduces with menses and then symptom free week 2. One or more of psychological symptoms - Depressed mood - Emotional lability - Anxiety / on edge - Irritability / anger affecting interpersonal relationships 3. One or more of the following up to a combined 5 symptoms - Anhedonia - Hyper or insomnia - Increased or decreased appetite or cravings - Lack of concetration - Lethargy / reduced energy - Being overwhelmed / out of control - Physical symptoms such as bloating, breast tenderness, joint or muscle pain, weight gain 4. Symptoms associated with significant distress on work, school or interpersonal relationships 5. Not an exacerbation of an underlying psychiatric disorder 6. Not assoicaited with other medical conditions or drugs 7. confirm diagnosis with at least 2 symptomatic cycles with daily ratings

Answer 316

Some women are sensitive to progesteorne Serotonin and GABA are involved. Serotonin receptors are responsive to oestrogen and progesterone and SSRIs are proven to reduce PMS symptoms GABA levels are modulated by the metbaolite of progesteroen, allopregnalone and in women with PMS these levels are reduced

Answer 317

First line - Exercise (some benefit) - CBT (comparable to fluoextine) - Vit B6 - COC (cyclical or continuous) - drosperinone (Yasmin - not subsidised in NZ). Better than other progesterones which can mimic PMS symptoms. Drosperenone is derived from spironolactone (blocks aldosterone action) - results in counteraction of estrogen-induced stimulation of RAAS that leads to sodium and water retention and symptoms such as breast tenderness and eodema. Drospierinone also has anti-androgenic properties. Use continuous rather than cyclically - Continuous or luteal phase (day 15-28) low dose SSRIs, e.g. citalopram / escitalopram 10mg - should be considered as one of the first line treatments especially for severe PMS. Appears to be effective for both psychological and physical symptoms. SE: nausea, reduced libido, somnolence, insomnia. Good evidence for luteal dosing only. Can stop in pregnancy as PMS symptoms will resolve. Taper if taking continuously. Second line - Estradiol patches (100mcg) and micronised progesterone (100-200mg) (day 17-28) orally or vaginally or Mirena. Estrogen amounts sufficient enough to supress ovarian activity. Need to combine with progesteorne to avoid hyperplasia. - Higher dose SSRIS continuously or luteal phase e.g. citalopram/escitalopram 20-40mg Third line - GnRH analogues + addback HRT (if using for more than 6 months). Highly effective. Supresses ovarian steroid production, causes decreased bone mineral density. If doesn't work then diagnosis is likely not right. DEXA scans every year, stop treatment if BMD declines significantly. Loss in BMD can occur after 6 months. Fourth line - Surgical treatment +/- HRT. TLH BSO. Consider when medical management failed, long term GnRH analogue is required or other gynaecologicla conditions indicate surgery. Can have oestrogen replacement without progesterone then. Always test with GnRH analogues first to ensure it will be beneficial. Shouldn't do BSO alone as will require progestoerne addback therapy which may exacerbate symptoms. Diuretics can be used for treatment of physical symptoms: in particular reduces weight gain, some beenfit in mood symptoms, antagonist of aldosterone. PROGESTERONE IS NOT HELPFUL on its own

Answer 318

10-15% (85% should have concieved after one year of UPSI, 92% after two years) Definition: 1-2 years of UPSI with no conception Fecundity: monthly chance of getting pregnant. 20-35% chance

Answer 319

35% female 35% male 10% mixed 10-20% unexplained

Answer 320

I: minimal: small number of superficial implants II: mild: more implants, some deeper III: moderate: small endometriomas in one or more ovaries, deeper implants, minor adhesions IV: severe: large endometriomas in one or more ovary, deeper implants, severe adhesions, bowel disease, bladder disease, obliteration of POD

Answer 321

Age Obesity (BMI >30 significant increase in infertility) Pelvic infections Endometriosis - Stage I-II, definite evidence improves fertility following - Stage III - IV, consider if endometriomas >3cm, pain / other symptoms present. Some say good evidence, some say poor evidence for improvement in fertility following this. Risk of impairment of ovarian reserve Fibroids - >2cm SM - >5-8cm IM - substantial size if SS RANZCOG recommends removal of fibroids if undergoing ART and have SM fibroids, have SM fibroids, infertility and symptoms related to fibroids such as HMB/ or pressure symptoms, multiple failed cycles where women has IM fibroids. - Reason: space occupying lesion, inflammation, diversion in blood flow

Answer 322

``` Morphology 4% Motility 40%, 32% progressive Count 40mil/ejaculate or 15mil/mL Amount - at least 1.5mL Vitality 58% ``` ``` Oligozoospermia: low count Asthenozoospermia: low motility Teratozoospermia: low morphology Oligoasthenoteratozoospermia: low in all 3 Azoospermia: no sperm in ejaculate Aspermia: no ejaculate ``` Normozoospermia: normal

Answer 323

1. Obstructive (30%) - CBAVD - STIs - Mumps - Tumours - Vasectomy 2. Testicular cause - Undescended testes - Torsion, orchitis, injury - CTX, RTX - Klinfelter syndrome XXY: hypogonadism, tall, gynaecomastia, lack of facial hair, mild intellectual disability, aggresive, antisocial behaviour - Y deletion (10%) - can do ICSI 3. Pre testicular cause - Hyperthryoid - Kallmans syndrome: many different genes invovled. Anosmia, increased PRL and androgens, hypothalamic hypogonadism. Treat with HRT - Androgen intake - HEad trauma, surgery, irradiation 4. Retrograde ejaculation 5. Smoking, medications, lifestyle, chronic medical conditions, psychosexual issues 6. Ejaculation or erection issues

Answer 324

Day 21 Progesterone. Should be >15 to indicate ovulation. <30 = likely suboptimal Day 3 FSH - should be <10. Peaks at day 3. (elevated in low ovarian reserve because follicular depletion = less oestradiol and inhibin feedback so increased FSH without change in LH. Day 3 E2: not a great marker. NICE doesn't recommend it. If high worse prognosis for ART. Rises in older women. Should be low at this time. Antral follicle count - should have 3 - 10 follicles in follicular stage AMH - equal to antral follicle count. If low = poor ovarian reserve. Related to poor response to ovulation induction. AMH inhibits primoridal follicles from being recruited to primary follicle, it decreases the sensitivity to FSH. COC decreases AMH over the following 6 months. Doesn't reflect egg quality

Answer 325

I - hypothalamic - pituitary failure: anorexia, excessive exercise, idiopathic hypogonadtrophic hypogonadism or Kallmans if associated with anosmia. Treatment: gain weight, reduce exercise. Ovulation induction with LH or FSH or pulsatile GnRH GnRH, FSH, LH, oestrogen all low II: hypothalamic - hypogonadotrophic - ovarian dysfunction. PCOS. ovulation induction with clomiphene, letrozole +/- metformin, OR gonadotrophins or ovarian drilling. FSH low or normal, LH high or normal, oestrogen low or normal III: ovarian failure - POI. Only way to get pregnant is with donor egg and IVF IV: Hyperprolactinaemia. affects pulsatility of GnRH so FSH and LH are low, oestrogen low, prolactin high. Treat cause, then can get pregnant spontaneously once PRL normal

Answer 326

Aromatase inhibitor Stops conversion of androstenedione and testosterone to estrone and estradiol peripherally (granulosa cells) This means less negative feedback to pituitary and increased FSH resulting in increased recruitment of follicles Give 2.5mg - 7.5mg daily from day 3 - 7 Aromatase inhibition decreases over time, increased oestradiol production, more negative feedback to FSH meaning less FSH and then primordial follicles undergo atresia and one primary follicle dominates. This results in mono-oocyte ovulation. Try for 3 - 6 cycles and then change tact if required Aromatase inhibitor doesn't act centrally Benefits over clomiphene less risk of twins (3.4 vs 10%) No direct anti-oestrogenic effect on ednometrium or cervical mucus Shorter half life so less risk of teratogenicity Lower estradiol levels systemically - better for women who have endo or breast cancer previosuly Birth rates 30 vs 20% Less SE About 20-40% of women will get pregnant and have a child after 3-4 cycles Have sex when largest follicle >18mm Quality of cervical mucus best just before LH surger

Answer 327

Selective estrogen receptor modulator Mixed anatagonist and agonist Blocks estrogens effect centrally so increased FSH is produced Recruits more follicles Becasue clomiphene has a long half life it hangs around and continues to block estrogen negative feedback to FSH. This means multiple follicles and multiple ovulation Give day 3 - 7 Twins 10% risk Triplets 1% OHSS <1% Also blocks estrogen receptors in cervical mucus making sperm harder to swin through

Answer 328

Used for PCOS women who letrozole / clomiphene / metformin hasn't worked OR hypothalamic hypogonadotrophic hypogonadism Start FSH injections daily shortly after spontaneous bleed or progesterone induced bleed Start at a low dose e.g. 37.5 IU / day for 2 weeks and then slowly uptitrate by 37.5IU a week until you notice at least one follicle >10mm then can stay on that dose? Scan every 2 -3 days. Once one to two follicles are >18mm can give HCG as trigger to ovulate (5000IU). If ≥3 follicles >15mm, need to stop and restart another cycle becasue too high risk for a multiple pregnancy Need to give GnRH agonist or antagonist at the same time to stop ovulation secondary to increased oestradiol in mid follicular phase and therefore switch to positive feedback GnRH agonist: Zoladex as a SC implant, nasal spray. Achieves pituitary downregulation by continuous adminsitration GnRH antagonist: prevents LH and FSH release e.g Ctrorelix (If doing IVF and egg pickup: give trigger (HCG or GnRH agonist) and then pickup 36h later

Answer 329

tubal factor infertility unexplained infertility preimplantation genetic diagnosis required severe male factor infertility using donor oocytes e.g. POI AMA and fertility preservation is important 20% change of live birth with each cycle 27% chance of live birth with each embryo transfer

Answer 330

Start FSH injections daily shortly after spontaneous bleed or progesterone induced bleed Start FSH day two of cycle Need to give GnRH agonist or antagonist at the same time to stop ovulation secondary to increased oestradiol in mid follicular phase and therefore switch to positive feedback GnRH agonist: Zoladex as a SC implant, nasal spray. Achieves pituitary downregulation by continuous adminsitration. Give from day 20 cycle prior until day 10 GnRH antagonist: prevents LH and FSH release e.g Ctrorelix. Give from day 6 of current cycle - this is what we normally use. Scan every 2 -3 days. Once one to two follicles are >18mm can give HCG as trigger to ovulate (5000IU). pickup 36h later HCG mimics LH surge Helps granulosa cells leutenise, final oocyte maturation and resumption of meiosis II Can also give GnRH agonist as trigger if lots ond lots of follicles becasue less likely to cause OHSS than HCG trigger GnRHantagonist cycle less OHSS (by 40%) If freezing then give oestrogen for 14 days, TVUSS to confirm 9mm trilaminar endometrium and then progesterone for 5 days and then embryo transfer

Answer 331

≤39 BMI ≤35 at referral and ≤32 at first treatment NZ citizien, resident, or work visa for 2 years Non smoker for 3 months No more than 2 children under the age of 12 at your house Trying for >1 year OR known female or male factor infertility OR need preimplantation genetic diagnosis OR need fertility preservation Partner BMI <40 Age <55

Answer 332

``` Ovulation defects Sperm abnormalities Tubal factors Endometriosis Unexplained fertility for how long Other factors such as cervical abnormalities, fibroids ```

Answer 333

blunted LH response (to increase TRH) and PRL increases Abnormal pulsatility of GnRH secondayr to increased PRL SHBG activity decreases so testosterone and oestrogen increased free fraction but overall decreased

Answer 334

Mild 33% of IVF moderate to severe 5% admission 0.5%

Answer 335

Hyperstimulated ovary, HCG trigger --> releases proinflammatory mediators, including VEGF This results in vascular permeability and results in third spacing of fluid, mostly ascites It also results in parodoxically hypovolaemia, hypoosmolar blood volume but a 20% drop in blood volume. Risks - Third spacing - Thrombotic events

Answer 336

Symptoms - Onset following HCG trigger or in early pregnancy - (ask when trigger was, HCG or GnRH agonist, how many follicles on last scan, how many eggs collected, hx PCOS or OHSS) - Breathlessness - decreased UO - Ascites, abdo pain, increasing girth - swelling vulva / leg - VTE - N+V Exam - Resp: pulmonary oedema, pneumonia, pleural effusion - Abdo: mass, ascites, wide girth (measure), abdo tenderness, peritonism (think something else) - Legs / vulva - General: weight, obs, dehydration Ix - Hct - HCG - FBC - U+es, including plasma osmolality - Coags (fibrinogen increased) - Biochem: albumin decreased, transaminases increased - Renal function - may get AKI - CRP: infection - ABG? pelvic USS +/- CXR

Answer 337

Early: within 9 days of tigger HCG, usually mild and self limiting up to 10/7 Late: usually more than 9/7 from trigger and is set off by endogenous HCG from an early pregnancy. Higher morbidity, can last weeks to months

Answer 338

Mild: mild abdo pain and bloating, ovaries <8cm Moderate: moderate abdo pain, ascites on USS, ovaries 8-12cm, N+V Severe: clinical ascites or hydrothorax, ovaries >12cm, hct >0.45, Low sodium, low serum osmolality, high K+, oliguria, low albumin, Critical: WCC >25, Hct >0.55, tense ascites, oliguria / anuria, VTE, ARDS

Answer 339

Mild to moderate and some severe cases can be managed at home - Strict fluid balance: drink to thirst, but at least 1L/day. Monitor input and output. If <1L / day of urine or >1L +ve fluid balance consider admission - Mobilisation, sometimes given clexane for home - Consider bloods if worsening symptoms (Admission if Hct >0.45) - Daily weight and abdominal girth (if >1kg weight gain admission) - Daily symptoms check - if pain not managable at home for admission - No NSAIDs Admit if - Increasing girth / weight - Fluid balance abnormalities as above - Intractable vomiting - Worsening pain - Worsening SOB - Tachycardic or hypotensive - Bloods: Hct >045, hyponatraemia, hyperkalameia - Decreased mobility Admission - Fluid resuscitation if required (1L NS then slow fluids to maintain 20-30mL/hr of UO) - VTE prophylaxis - Daily symptom check, weight, girth measurements - Fluid balance chart - Daily bloods - Consideration of albumin if severe albuminaemia - Consideration of ascitic tap if required

Answer 340

Individualised FSH dosing Frequent USs and oestrogen levels to monitor response Use of GnRH agonist for trigger instad of HCG for high responders Freeze all approach Only transfer one embryo if transferring Can give cabergoline on day of trigger to reduce VEGF release Progesterone luteal support instead of HCG Metformin use during stimulation for women with PCOS

Answer 341

Agenesis / hypoplasia: vaginal, cervical, fundal, tubal, mixed Unicornuate: communicating, non-communicating, no cavity, no horn Bicornuate Didelphys Subseptate Arcuate DES related Incidence 7%????

Answer 342

Wolfian: SRY gene --> gonad differentiates to testes - YS sends primordial gametes to testes - Sertoli cell make testosterone which stimulates Wolfian ducts to form - Leydig cells makes AMH which inhibits Mullerian ducts - Wolfian duct creates: seminal vesicles, vas deferences, epididymis, common ejaculatory duct - Testosterone is formed into dihydrotestosterone which stimulates external genitalia by 6-7 / 40. Genital tubercle to glans, labioscrotal swelling to scrotum, urogenital ridge to prostatic urethra etc, urethral fold to shaft Mullerian - No SRY gene so gonad differentiates to ovaries - YS sends oocytes - Oestrogen and progesterone formed in follicular cells - No sertoli cells so no testosterone so no Wolfian ducts - No leydig cells so no AMH so no inhibition to mullerian ducts - Mullerian duct forms uterus, cervix, tubes, upper 2/3 of vagina - Oestrogen stimulates external genitalia: genital tubercle to clitoris, labioscrotal fold to labia, urogenital fold to urethra, skenes, bartholins, urethral fold to labia minora

Answer 343

40% renal | 20% spinal

Answer 344

``` Imperforate hymen Transverse vaginal septum Cervical +/- vaginal agenesis Obstructed hemivagina with didelphys uterus Non communicating rudimentary horn ``` Presents with primary amenorrhoea and cyclical pain or severe dysmenorrhoea not improved with usual treatments

Answer 345

Mayer Rotikansky Kuster Hauser syndrome (MRKH) Complete mullerian agenesis Many genes possibly involved Normal ovaries No uterus, tubes, cervix, upper 2/3 vagina 40% renal tract abn CAIS: compelte androgen insensitivity syndrome X linked recessive disorder Karyotype XY Testosterone produced but abnormal androgen receptor No Wolfian duct Leydig cells still produce AMH so Mullerian duct doesn't develop Normal female external genitalia, scant pubic hair Normal breast development becasue of peripheral aromatization of testosterone Small gonads inside pelvis - 5% risk malignancy in childhood, 15% in adulthood. Remove 16-25y after growth spurt.

Answer 346

Unification error: failure of two sides to join appropriately - Unicornuate, bicornuate, Didelphys: PTB 50%, FGR 50%, Malpresentation 50%, CS 66% - Rupture rudimentary horn Canalisation error: failure of removal of fused area in middle - Subseptate: miscarriage 44%, PTB 25%, FGR 12%, malpresentation 16%, CS 45% - Arcuate subset of normal - Longitudinal vaginal septum: labour dystocia, rupture in labour.

Answer 347

Ambiguous genitalia - CAH - Partial androgen insensitivity syndrome Genitalia discordant with chromosomes - Complete androgen insensitivity syndrome 46XY phenotypically female - Pure gonadal dysgenesis - Swyers syndrome 46XY phenotypically female

Answer 348

8-12 girls 9-13 boys Delayed: >13 thelarche, >3y menarche from thelarche Average age menarche 12.8 Order of puberty: thelarche, pubarche, growth spurt, menarche and adrenarche, change to adult body shape, full breasts

Answer 349

``` Home / environment Education / employment Activities Drugs Sex Suicide / depression ```

Answer 350

Hypergonadotrophic hypergonadism Idiopathic / genetic in 80% of cases Otherwise - Tumour - SOL - Injury to head - Hydrocephalus causing excessive pressure on hypothalamus - Excessive exposure to sex steroid hormones e.g CAH or central McCune Albright syndrome - Infection / inflammation e.g. encephalitis Children are taller than their peers (eventually shorter) Advanced bone age - do wrist x-ray ``` Tests - FSH, LH (high) - TFTs - PRL - MRI head - USS pelvis: uterine age, ovarian appearance, adrenals - Bone age x-ray - Oestradiol, testosterone, DHEA-S, progesterone , 17OH prog FBC Electrolytes ``` Gold standard: GnRH stimulation test: LH:FSH ratio >8 = positive. ``` Treat with leuprolide or goserelin 3-6 monthly checks annual boen age x-rays Stop age 10 -11 - ```

Answer 351

Ruling made in 1980 based around contraception use in 14 - 16yo Child must be deemed competent to make the decision - child's age, mental capacity and maturity - understand the treatment - understand the risks assoicated with the treatment - Ensure understand the advice given - Ensure they understand alternate options - Have the ability to explain rationale behind this reasoning and decision

Answer 352

Applied specifically to advice around contraception use in 2006, added in to encompass TOP and STI treatment - Must understand the professionals advice - Cannot be persuaded to tell their parents - Likely to be having sex with or without contraception - Possible physical or mental harm if don't prescribe the contraception - In their best interests

Answer 353

No menstruation by age 15-16 with normal secondary sex characteristics No secondary sex characteristics by age 13 Ix if - No menarche by age 15 and normal secondary sex characteristics - No menarche 3y after breast development - No menarche but hirsutism, excessive exercise, anorexia or outflow tract obstruction suspicion - No breast development by age 13 Secondary amenorrhoea: absent periods for 6/12 following a period of normal regular menstruation or 12/12 if irregular periods prior

Answer 354

Brain - encephalitis, altered consciousness, seizures Eye Nose: anosmia Oeophagus Lungs: ARDS, pneumonia, resp failure Heart: pericarditis, myocarditis, heart failure, MI, arrhythmia Pancreas: beta cell dysfunction, pancreatitis Colon: diarrhoea Small intestine: diarrhoea Liver GB Kidney: AKI, ATN Blood vessels: endothelial dysfunction, microthrombosis, vascular inflammation, vasospasm

Answer 355

FSH >20IU/L on 2 occasions 4 weeks apart, in context of amenorrhoea

Answer 356

Genetic - Turners - Fragile X - Somatic mutations - Other defects in X chromosomes Autoimmune - Isolated - Associated with Addisons disease or polyglandular syndrome Toxins - CTX - RTX - Galactosaemia - Infections e.g. mumps Surgery - Bilateral oophorectomy - Hysterectomy with resulting abnormal blood supply to ovary

Answer 357

XO or XX mosaic Abnormal migration of primordial cells to ovary and accelerated loss 20% will spontaneously go into puberty 10% will spontaneously finish puberty 1% will ovulate 95% will die in utero Incidence doesn't increase with maternal age Reduced life expectancy ``` Pitting oedema at birth associated with cystic hygroma Normal intelligence Normal mullerian tract HEart defects 50% - most common cause of death. Coarctation of aorta, AV abnormalities Renal anomalies Short Webbed neck low hairline Autoimmune disorders such as diabetes and thyroid disease widely spaced nipples facial stigmata micrognathia, ptosis, prominent ears ```

Answer 358

VMS: can last decades but on average 4-5 years - hot flushes, night sweats GU symptoms: arrive about 4-5 years following menopause - Vaginal dryness, dyspareunia, atrophic vaginitis, decreased glycogen so decreased lactobacilli, pH increased to 6-7, more susceptible to infection, decreased detrusor contracility, increased residual, increased frequency, nocturia, urgency, oceractive bladder, labia and vulva lose their fullness, introitus narrows, mucosal surface inflamed metabolic issues - Increased abdominal obesity, T2D, IGT, hyperlipidaemia Cardiovascular changes: endothelial dysfunction, hyperlipidaemia skeletal: increased bone turnover, increased fractures neurological: congnitive impairment Physical: fatigue, headaches, myalgias, arthralgias Psychological: depression, anxiety, sleep issues, irritability, memory, concetration

Answer 359

``` Unexplained vaginal bleeding Active liver disease Personal hx VTE or strong FH VTE Coronary heart disease Stroke ```

Answer 360

``` Decreases VMS and urogenital symptoms ++ Decreases osteoporosis related fractures Decreases colon cancer risk Decreases alzheimers risk Oestrogen only MHT decreases CVD risk. Mixed does but not significantly, may lower chance of mortality. Doesn't decrease all cause mortality ``` - Decreases risk of osteoporosis and fractures, including hip fractures. Hypooestrogen increases osteoclast activity resulting in bone resorption, replacing oestrogen helps prevent this - Improves genitourinary syndrome: decreases vaginal atrophy and as a result dyspareunia, vaginal bleeding. Improves bladder health (hypo-oestrogenism leads to UTIs, urgency, nocturia, frequency) - Improves physiological symptoms: sleep, fatigue, headaches - Improves psychological symptoms: mood swings, irritability, anxiety, concetration - Reduced risk of colorectal cancer - Reduced risk of endometrial cancer when combined - Possible reduced risk of alzheimer’s disease

Answer 361

1. Breast cancer, 1 extra case per 1000 women / year. Progesterone drives this. No evidence micronized progesterone any better. Previous breast cancer = CONTRAINDICATION. No evidence oestrogen is linked to breast cancer. Continuous prog more risk c.f cyclical. Lifestyle, obesity, ETOH use all linked to breast ca also. Prog increases breast density 2. Endometrial cancer in unopposed oestrogen only. Risk persists once stopped 3. No increased risk of ovarian cancer 4. VTE / Stroke - Transdermal < oral - 2 fold increased risk - Prev VTE 10% risk recurrence. CONTRAINDICATED - Absolute risk is low 5. Cholecystitis

Answer 362

Advantages: easily taken, reliable Disadvantages: increased risk of VTE, increased risk of cholelithiasis, increases SHBG and thyroid binding globulin (may need to increase thyroxine dose) Options - Conjugated equine estradiol (permarin). Contains estrone, androgen, progestogen. From mares urine. half life 12h - 17Betaoestradiol - bio-identical: half life longer - Progynova: oestradiol valerate

Answer 363

Advantages - Avoids gut and first pass metabolism - Lower doses required - No increased risk of VTE or stroke risk - Convenient Disadvantages - Rash - Sticky - May forget to change Options 17B oestradiol: bioidentical hormone. Estradot. Climara Also pessaries or creams

Answer 364

Medroxyprogesterone acetate (provera) - Breast tenderness, bloating, mood changes - Breast cancer risk increased - Minor effect on coag parameters Norethisterone - Same as above - Dervied from testosterone so possible increased libido Micronized progesterone - Less SE - Possibly less risk of breast cancer but no good evidence - Biological progestogerone but micornized so is absorbed easier - No effect on coag parameters MIRENA

Answer 365

CBT decreases VMS Hypnosis decreases VMS Gabapentin 900mg nocte decreases by 60%, equivalent to MHT SNRIs venlafaxine decreases by 70% Escitalopram decreases by 50% Clonidine by 50% (alpha adrenergic agonist) Weight loss for obese women (exercise not proven) Try for 6/52 and then cahnge if no symptom relief, including for MHT COC in women <45 only

Answer 366

BRCA: after risk reducing surgery start with non hormonal options, can consider oestrogen if not working, after discussion of risks POI: COC if <45 Lynch syndrome: OK after risk reducing surgery Post menopausal cysts: BSO first Ovarian cacner with BSO: fine to use Breast cancer: NO Previous VTE: oral oestrogen contraindicated. Transdermal porbably okay. Pick one of progestogens with least VTE risk (e.g. micornized progesterone, Mirena), tibolone no increased risk Undiagnosed vaginal bleeding: NO Active liver disease / gallbladder disease: transdermal oestrogen only Hypertension: only once BP controlled with antihypertensives CVD: consult with cardiologist first. Transdermal probably okay Endometriosis: controversial Some recommend low dose oestrogen after hysterectomy, some recommend combined depiste hysterectomy. Tibolone okay Migraine: fine Obesity: transdermal patches reocmmended Porphyria: contraindicated Endometrial hyperplasia with hysterectomy: can give E alone. orE+P Cancers - Cervical: fine to have MHT - Early stage endometrial: fine to have MHT!!! - Stage III or IV endometrial cancer - not enough data to inform - Uterine sarcoma: not recommended, some ER and PR positive - Ovarian cancer: high grade serous, clear cell mucinous: fine - Ovarian cancer: low grade serous and endometrioid - not fine - Vulval and vaginal: fine - Breast cancer: no MHT. Consult with breast surgeon re vaginal methods - Colorectal cancer: fine - Lung cancer, ER positive: no consensus

Answer 367

HABITS trial: increased risk: E+P combined Stockholm trial: no increased risk - unopposed oestrogen or addition of long course progestogen If need it then lowest dose oestrogen possible and preferably micronized progesteorne cyclical. Mirena - not enough evidence yet Tibolone - likely same risk as MHT MHT with aromatase inhibitors - not enough evidence MHT with SERMS - not enough evidence Ovestin: probably fine. Try vaginal lubricants first

Answer 368

``` 75% asymptomatic Average age 63 50% smoked Obese 1/3 hypertension Some had previous dx CVD On average 12-15y post menopause - vascualr changes already happened! Poor statistical methods Lots of confounders Not blinded Information sent out about the detrimental effects of MHT, lots of drop outs ```

Answer 369

45 - 59 normal <45 = early <40 = POI

Answer 370

JAMA 2002 Multicentre RCT, "double blinded" ITT 16000 women E+P (CEE and MPA) vs placebo Primary outcome: coronary heart disease Primary adverse outcome: breast cancer Other outcomes presented as a global index score - fractures, colorectal cancer, endometrial cancer, stroke, PE, DVT, death Stopped just after 5 years because - breast cancer rates exceeded safe threshold - global index score indicated more risk than benefit ``` Results (hazard ratio) CHD: 1.29 Breast ca: 1.26 (CI crossed 1) CRC reduced 0.63 Endometrial cancer reduced 0.83 PE: 2 Hip # 0.66 No difference in all cause mortality ``` Criticisms - Average age 63 - Majority >10y from menopause - 1/3 hypertensive - Some previous dx CHD already - 50% smokers - Good proportion obese - 75% asymptomatic - Lots of confounders - Lots unblinded - Some given information about risks of E+P so stopped

Answer 371

``` JAMA 2004 10,000 women E only vs placebo Inclusions: no uterus, 50-69yo Exclusions: any medical condition which predicted survival <3y, active breast or other cancers within last 10y ``` RCT, blinded, ITT, multicentre Primary outcome: CHD - no change - Stroke increased risk by 39%, not ss VTE increased risk by 33% ss Secondary outcomes - Breast cancer, reduction but not ss - Reduced hip and vertebral and all # - No diff CRC or other cancers Stopped after 7 years -

Answer 372

Cohort study Lancet 2003 Million women - questionairre: mHT use, sociodemographic, timeline of menopause Followed for 2 -4 yr ``` Results Overall increase in breast cancer incidence RR 1.66 (decreased to 1 after stopping MHT) Estrogen only: RR 1.3 E+P RR 2 Increased mortality from breast cancer ``` Risk of death from breast cancer RR 1.22, RR 1 for past users For 5 years of use <65y: 6/1000 extra cases with E+P 1.5/1000 extra cases with E Strengths: Huge study Cancer registry and prospective study so no recall bias Limitations: Million women study participants slightly more likely to use HRT than general population and come from less deprived areas (although this should not bias internal comparisons within the cohort) Use of HRT reduces sensitivity of mammography, therefore increasing the probability that a breast cancer is diagnosed as an interval rather than at screening.

Answer 373

DCDA ≤3/7 1/3 MCDA ≤8/7 2/3 MCMA ≤13/7 1-2% Conjoined >13/7

Answer 374

10-15% of Monochorionic twins

Answer 375

2% DCDA | 8% monochorionic (placental issues, increased risk of anomalies, TTTS)

Answer 376

Imbalance in arterial vascular anastamoses Results in imbalance of haemodynamics and resulting changes in endocrinology Donor: hypovolaemia, hypoperfusion so increases renin, oliguria / anuria, oligohydramnios, eventually abnormal UAPI with redf REcipient: hypervolaemia, decreased ANP. polyhydramnios, cardiac failure, hydrops, dv with reversed a wave

Answer 377

I: oligo / poly (90% survival - expectant management) II: donor bladder not seen over 60 minutes, dopplers can be abnormal but not critically so III: critically abnormal dopplers. UAPI redf donor, DV reversed a wave recipient IV: hydrops V: death II - IV - fetoscopic laser photocoagulation selective or solomons technqiue (divide in two) Difficulties: anterior placenta, separation of membranes, advanced stage, selective FGR Survival of both twins = 65% survival of one twin = 85% Risk of abnormal neurodevelopmental outcome = 9% - CP - IVH Higher risk if recurrent TTTS, TAPS or extreme prematurity or PPROM Amnioreduction can be done but 40% risk loss TOP of pregnancy if remote from viability considered ``` Selective termination (cord ligation) if one has anomalies for example 20% risk of cotwin demise ```

Answer 378

Twin anaemia, polycythaemia sequence 5% of MC twins 10% of MC twins after laser Miniscule vascular anastamoses with slow transfusion donor: anaemia, sometimes cardiomegaly, sometimes growth restriction recipient: polycythaemia Do weekly USS from 16/40 if growth discrepancy or one twin <10th. Otherwise from 20/40 MCA >1.5mom in donor 5 stages Mx - poor evidence to guide ?>32 - just deliver ?28-32 - consider IUT to buy time ?<28 - fetoscopic laser. 10% recurrence. Do solomon technique. TEchnically harder than TTTS. Mortality 9% (Donor > recipient) 18% post laser TTTS TAPS

Answer 379

10-15% of MC twins 50% TTTS Unequal sharing of placental mass >25% discordance or <10th EFW of one twin Usuauly starts around 20/40 3 types I: discrepancy but positive end diastolic flow in dopplers. Unequal sharing of palcental mass but large anastamoses which decrease the risk. 90% survive. Delivery 32-34 weeks. Weekly scans. OP management II: absent or reversed end diastolic flow in one twin. smaller anastomases. Very unequal sharing. Delivery by 32 weeks. Needs inpatient monitoring, twice weekly scans, BD CTG. Often need to deliver earlier. 30% risk IUFD III: cyclical changes in diastolic flow (absent, reversed, positive). Delivery by 32 weeks as above. Large arterial anastomoses. 10-15% risk IUFD and 10-15% risk brain injury co-twin Treatment - Selective reduction - Sometimes laser - Majoirty of time just delivery

Answer 380

Twin reversal arterial perfusion sequences After one twin dies 1 % of MC twins Pathophysiology – Early demise of one twin in MC pregnancy Large AA anastomosis “Pump” twin perfuses the “acardiac” twin via large AA anastomoses Over time, risk of high output heart failure and demise of pump twin; Risk of polyhydramnios and preterm birth. Always do an MRI to check twins brain after a cotwin demise Can do laser or cord coagulation of dead twin

Answer 381

DCDA: 37 MCDA: 36-37 MCMA 32 - 34 - CS. High risk fetal death in labour MCTA or DCTA: 35 MCMA triplets or MCDA triplets individualised

Answer 382

NEJM 2013 Multicentre RCT Not blinded 2800 women Inclusion: DCDA or MCDA pregnancy. 32 - 38+6. 1500g - 4000g. leading twin cephalic. both alive Exclusion: fatal anomaly, reduction >13/40, leading twin not cpehlaic, contraindication to labour, MCMA Primary outcome: neonatal mortality or serious morbdiity Secondary: 2y neurodevelopmental outcome or death No ss differences 60% in vaginal group had VB 90% in CS group had CS Limitations Subgroup analyses not powered to detect difference in those outcomes Only generalizable to centers where CS facilitated within 30mins AND experienced obstetrician can be present for vaginal delivery Not stratified out by prev CS ``` Strengths Multi center RCT High numbers Good follow-up Included DCDA and MCDA Across gestations including spontaneous preterm birth ```

Answer 383

Increased pigmentation: aerolae, axilla, linea nigra. E and P stimulates melanocytes to produce excess melanin Melasma: brown spots on forehead, cheeks, chin - as above Spider naevi: on face, upper trunks and arm. Palmar erythema: 70% of women. Fades after delivery Hair loss (telogen effluvium): occurs PP in most women 4 - 20 weeks after delivery. Increased conversion of hairs from the anegen (growing) to telogen (resting) phase, following increased proportion of hairs in anegen phase during pregnancy. Hair is lost diffusely but recovery is usual within 6 months. Striae gravidarum: more common in obese women and multiple pregnancy. Appear perpindicular to skin tension lesions as pink linear wrinkles. Fade and become white and atrophic but never disappear completely Reduction in CMI influences susceptibility to skin disease and skin infections Pruritis common Hypertrichosis: increased hair growth in a non hormonal pattern. Hirsutism: hair growth in male pattern ?increased circulating androgens in pregnancy Nail changes: increased brittleness, leukonychia, splitting, ingrown toenails, increased growth etc....... Glandular changes: hyperhidrosis and millaria (heat rash), sebaceous gland excretion, lubrication to nipples and aerolae Th1 --> Th2 shift so skin conditions that are th1 driven such as psoriasis are improved, eczema which is th2 driven worsens

Answer 384

Most common pregnancy specific dermatoses Incidence 1/200 Stretching of the skin elicits an immune response due to connective tissue damage Onset 3rd trimester More common in primips or multiples Distribution: umbilical sparing, adbomen, along striae, spreads to thighs, buttock, under breasts and upper arms. Pruritic, urticarial papules, often red with pale halo around each papule. Coalesce to form large urticarial plaques and occaiosnally small vessels (but not bullae) Resolves rapidly after deliver No effect on the fetus are known Treatment - Menthol (1%) in aqeuous cream - Antihistamines - Hydrocritosone 1% (sometimes stronger are needed) - Ssytemic steroids in rare cases Recurrence is rare and often mild

Answer 385

Incidence 1:10,000 - 1:60,000 Serious condition Occurs anytime from 9 weeks to 1 week postpartum, usually in 3rd trimester though Pimrips and Multips UMBILICUS AFFECTED. abdo, limbs, palms, soles Eruption of intensely pruritic urticarial erythematous papules and plaques, target lesions and annualr wheals. 2/52 later vesicles and large bullae appear Often improves in 3rd timester if had it earlier, flare PP Sometimes develops into bullous pemphigoid Pathogenesis: autoimmune, possible related to exposure to fetal antigens. AIgG binds to a protein int he basement membrane of the skin which triggers an immune response leading to formation of subepidermal vesicles. the normal function of this protein is to stick the dermis and epidermis together Usually exacerbates and then remits Lesions resolve weeks to months following pregnancy Associated with AI conditions - grves, T1D, RA Dx: skin biopsy and direct immunoflourescence which shows complement deposition on BM. Fetus: low BW, PTB, SB, similar bullous reaction on fetus Treatment - Potent topical steroids or very potent (dermol) Most require systemic steroids oral antihistamines Can use azathioprine, cyclosporin, IVIGG, plasmaphersis Usually recurs earlier, and with COC

Answer 386

eczematous changes at typical atopic sites - flexor surfaces etc nil effect on fetus emollients with menthol, benzoyl peroxide, topical steroids, antihistamines, phototherapy 1/300

Answer 387

eczema: th1 --> th2 predominant Acne: increased circulating androgens, blocked sebaceous glands

Answer 388

Plasma volume increases by 50%, red cell mass by 30%: relative anaemia from haemodilution - fall in Hb, Hct, red cell count Platelet count drops - thrombocytopenic when <100 No change in MCV or MCHC 3 fold increase in iron requirements for red cell synthesis, enzyme and fetus 10-20 fold increase in folate requirements 2 fold increase in B12 Hypercoaguable state!

Answer 389

Malaria most common second most common worldwide: Folate deficiency: 25% of pregnant women won't have an appropriate diet to prevent megaloblastic anaemia. Haemolytic anaemia, sickle cell disease, thalasaemia and hereditary spherocytosis all increase risk of folate deficiency. ETOH consumption, azathioprine use. iron deficiency anaemia B12 deficiency less common - dietary deficiency normally - IBD, pernicious anaemia, coeliac disease, pernicious anemia. Causes very high LDH levels and pancytopenia. Ineffective haematopoiesis results in megaloblastoid changes of th erythroid precursors in bone marrow. Destruction of these early red cells in the bone marrow causes the riased LDH and bilirubin Autoimmune disorders - SLE Infections Malignancy

Answer 390

Adverse effect on iron dependent enzymes in each cells has profound effects on muscle and neurotransmitter activity Associated with low birthweight, preterm delivery, increased blood loss at delivery Iron supplementation is proven to decrease iron deficiency anaemia but has no ss differences in low birthweight newborns and preterm births. No differences in neonatal deaths or congenital anomalies.

Answer 391

``` Previous baby with NTD Personal history NTD Obesity AEDs Diabetes on insulin Haemolytic anaemia Sickle cell anaemia Other anaemias Known malabsoprtion syndromes Previous folate deficiency ```

Answer 392

The current conditions screened for are: ``` amino acid disorders (eg, phenylketonuria (PKU) and maple syrup urine disease) fatty acid oxidation disorders (eg, MCAD) congenital hypothyroidism cystic fibrosis congenital adrenal hyperplasia galactosaemia biotinidase deficiency severe combined immunodeficiency (SCID). ```

Answer 393

Includes Sickle cell anaemia HbSS, as well heterozygosity with other abnormal haemoglobins e.g HbSC, HbSB Carrier: HbAS Most common inherited condition worldwide: Africa, Carribean, Meditteranean Sickling of the red cells is precipitated by infection, hypoxia, dehydration, acidosis Causes 1. Vascular occlusive crises with ischaemia and pain 2. Spleen sequestration of red blood cells 3. Aplastic anaemia ``` Acute vaso-occlusive crises Anaemia: haemolytic Splenomegaly and infarction Acute chest syndrome: fever, tachypnoea, pain - etc from infectino or infarction from intravascaulr sickling or thrombosis Splenic sequestation Gallstones Retinopathy Stroke ATN Leg ulcers Necrosis of bone Pulmonary hypertension ``` Diagnose by electrophoresis Crises complicate about 35% of pregnancies Perinatal mortality increased by 4-6 fold (2.5%) Increased risk of miscarriage, FGR, PTL, PET, abruption, APH, fetal distress, CS, infection, thromboembolic events Sickling infarcts in placenta, maternal anaemia, increased blood viscosity Prepregnancy - Partner screening and PGD - Sometimes CVS, amnio, FBS - ECHO: exclude pulmonary hypertension!! - Renal and LFTs annual - Retinal screening - Iron overload: MRI to assess body iron loading. Aggresive iron chelation before conception is significantly overloaded - Screen for red cell ab - Check up to date with vaccinations: encapsulated bacterial infections more common: N meningitides, S pneumoniae, haemophilus influenzae. Also Hep B, influenza, COVID Management - MDT - 5mg folic acid / day - Penicillin prophylaxis (penicillin V 250mg BD) - Pre-pregnancy genetic counselling - Paternal screening - Electrophoresis of level of HbF - higher the level the better - STOP hydroxyurea prior to pregnancy (used to decrease incidence of acute painful crises and acute chest syndrome outside of pregnancy - stop 3 months prior to conception as teratogenic in animals) - Often patients on ACEI / ARBs - stop / switch. - LDA - increased risk PET - Hb and MSU every visit - Regular growth scans - LMWH if admitted - Manage crises aggresively: admit, analgesia (opiates), adequate rehydration, antibiotics if infection, keep patients warm and well oxygenated, ABG or pulse oximetry is mandatory, oxygen if required. - q30min obs initally - WCC often raised in SCD - CXR: acute chest syndrome - infiltrates. - Blood transfusion if severe anaemia, splenic sequestration or in acute chest syndrome or stroke: alloimmunisation very common in SCD patients. Cross match for C, E and kell antigens too. - exchange transfusion if patient is volume replete and acute stroke or sickle chest syndrome - Exclude PE: CTPA because of abnormal CXR. Anticoagulaiton in interim - NSAIDs if 12-28/40 - MRI if neurological symptoms - Reticulocyte count: if low consider parvovrius and isolate. MFM referral. - Discahrge when pain under control - Deliver by 38-40 weeks - IOL. Cross match blood. Avoid dehydration, acidosis, sepsis, hypoxia!! Continuous sats monitoring. Low threshold for abx. PP - LMWH 7/7 for NVB, 6/52 CS - Contraception: progesteorne and non hormonal methods, COC as second line

Answer 394

4 genes 1 defective gene - silent carrier 2 defective genes - trait 3 defective genes - trait - likely has microcytic anaemia and poor oxygen delivery 4 defective genes not compatible with life - hydrops fetalis and IUFD Often need iron and folate supplements Don't give IV iron Prenatal diagnosis referral if both parents are alpha 0 (2 normal genes only) - risk of major. Sometimes need RBC transdusion

Answer 395

2 genes 1 abnormal gene = trait = microcytic anaemia 2 abnormal genes = major: regular blood transfusions required - alpha globin genes build up in RBC and haemolysis occurs as a result - iron (haemochromatosis), bilirubin released into blood - Jaundice - Haemochromatosis causes: cirrhosis, diabetes, growth retardation, hypothyroidism, pericarditis, arrhythmias. - Fatal without transfusions - Bloods show low Hb, low MCV, high reitculocytes, target cells. - Electrophoresis shows HbA2 (alpha x 2, delta x2) and HbF (alpha x 2 and fetal x 2) - Bone marrow production expands - enalrged forehgead and cheekbones. - Hepatosplenomegaly! - hypogonadotrophic hypogonadism - subfertility - cardiac failure 50% of deaths MRI methods for cardiac iron overload detectino and hepatic iron overload. BM transplantation can occur Pregnancy is very rare!! Treat with regular transfusions Iron chelating agents +/- splenomegaly (not routinely offered) Bet thalssaemia intermedia is when you have one abnormal gene but it just decreases production of beta chains doesn't completly stop it. usually survive without regular transfusions. Preconception care 1. MDT 2. Increased risk of cardiomyopathy 3. Increased risk of FGR 4. STOP iron chelation therapy with desferrioxamine prior to pregnancy - women can develop new endocrinopathies such as diabetes, hypothyroidism and hypoparathyroidism and hypogonadotrophic hypogonadism. Do aggresive chaltion in preconception stage. sometimes can use desferroxamine in 3rd trimester 5. HbA1c is not a good marker as likely just from donated blood - have to do serum fructosamine 6. Thyroid status: assess and start treatment if required 7. Cardiac function: ECHO, ECG, T2 cardiac MRI prior to pregnancy . Reduced EF relative contraindication to pregnancy 8. Liver: assess iron concetration with a ferriscan or MRI and assess gallbladder (common for cholelithiasis becasue of haemolytic anaemia) and cirrhosis! 9. Bone density scan to all women and serum vitamin D concetrations should be optimised with supplements if necessary - osteoporosis is common. Discontinue bisphosphonates 10. Red cell Ab - alloimmunity in 16% 11. Medication review: discontinue iron cehlating agents 3/12 out. Can use in low doses from 20/40 12. Hep B vacc if not immue 13. Determine Hep C status 14. If had spleenctomy: penicillin prophylaxis and vaccinate against H. influenzae, S. penumoniae, N meningitidis 15. Higher risk of NTDS - 5mg Folic acid Ovulation induciton may be reqiured Consider PGD if both parents carriers Pregnancy care 1. Mdt 2. Regular growth scans (from 24/40 monthly and then 2 weekly ffrom 28/40) 3. FGR a risk becasue of maternal anaemia and 4. Monthly assessment of fructosamine 5. Cardiac review 28/40 6. Monitor thyroid function 7. Aim pretransfusion Hb 100 if have major thalassaemia - worsening anaemia or FGR - 2-3U to maintain Hb >120. Monitor 2-3 weekly. 8. Aspirin if plt count >600 OR splenectomy 9. LMWH if plt count>600 and splenectomy - Prothrombotic tendency due to presence of abnormal red cell fragments, especially if undergone splenectomy. Intrapartum care - Deliver in hospital - No evidence for IOL if no other obstetric complications - Cross match! - Give desferrioxamine in labour if thalassaemia major - High amounts of iron may cause free radical damage and cardiac dysrhtymia whilst stress of labour!! - Continuous monitoring PP care - LMWH 7/7/ NVB, 6/52 CS - BF recommended - desferrioxamine fine as not orally absorbed

Answer 396

Rare Haemorrhagic and thromboembolic manifestations JAK2 mutation in some Pregnancy issues - Placental thrombosis, FGR Management - Spontaneous fall in platelet count common - Plt >600 --> aspirin to prevent aggregation and thrombosis - Interferon alpha okay to use in pregnancy Ohter cytotoxic agents not okay

Answer 397

``` Spurious result Gest thrombocytopaenia Immune thrombocytopenic purpura - more likely if documented low platelets in first half of pregnancy. Autoantibodies against surface antigens - platelet destruction by reticuloendothelial system - e.g. spleen HELLP DIC Sepsis Haemolytic uraemia syndrome / thrombotic thrombocytopenic purpura HIV, drug, infections SLE and APS BM supression and folate deficiency ```

Answer 398

fetal disorder caused by feto-maternal incompatibility for platelet antigens 1/2000 10% of neonatal thrombocytopenia

Answer 399

more likely if documented low platelets in first half of pregnancy. Autoantibodies against surface antigens - platelet destruction by reticuloendothelial system - e.g. spleen Diagnosis of exclusion No Ab determination available Capillary bleeding with counts <50 Spontaneous bleeding mucous membranes counts <20 Antiplatelet immunoglobin can cross placenta and cause fetal thrombocytopenia. Antenatal or neonatal intracranial haemorrhage 0 - 1.5% Best predictor: severe neonatal thrombocytopenia Maternal consideration - Exclude associated conditions such as SLE and APS - Plt count monthly, more freuqently in 3rd trimester - Treatment in first or second trimester if symptomatic with bleeding, count <20 or count needs to be increased prior to invasive procedure - <50 prior to delivery - treat - <80 - treat to facilitate regional anaesthesia - CS only for obstetric reasons - Corticosteroids first line 20-30mg / day then wean to lower dose to maintain count >50 - IVIG in resistant cases - Splenectomy in extreme cases - Penicillin if splenectomy previously - Azathiorpine, cyclosporin if prednisolone or IVIG not succesful - Plt transfusions as last resort becasue will increase antibody titres Fetal considerations - Transfer of IgG increases at end of pregnancy - baby not at risk of bleeding before labour and delivery - CS only for obstetric reasons - ICH not decreased with CS - Cord platelt count immediately after delivery (nadir 2-5 days later ehwn splenic circulation established) - Most haemorrhagic events occur 24-48 horus later. Give IVIG if <20 or symptomatic - Avoid FBS and FSE if plt count <80 in monther

Answer 400

High platelet count

Answer 401

Causes: haemorrhage, PET, HELLP, AFE, Massive infection, retention of dead fetus Clinical features: asymptomatic or massive haemorrhage Pathogenesis: procoagulant substances such as thromboplastin, phospholipid and those resulting from endothelial injury are released into circulation and casues stimulation of cogulation - production and breakdown of coagulation factors. consumption of clotting factors and platelets leading to bleeding Fibrinolysis is stimulated and fibrinogen degradation products interfere with the production of firm fibrin clots Decreased fibrinogen! Level <2 is signifcant. Thrombocytopenia Prolonged clotting time Blood looks watery Treatment - Manage underlying casue MTP Coagulopathy treated with FFP, red cells, plt if <80 and onging bleeding Cryoprecipitate: clotting factors recombinant fibrinogen is <1g/L and ongoing bleeding Recombinant factor VII consider - expensive!! Usually resolves 24-48h after delivery

Answer 402

1% incidence Autosomal dominant vWF - adhesive protein that has an important role in platelet function and stability of FVII. Required for binding of platelets to subendothelium after vessel injury When abnormal, platelets can't bind Complete or partial deficiency APTT prolonged vWF and FVIII may be reduced Pregnancy can lead to normalisation of vWF and FVIII levels with a fall in postpartum Effect of vWD on pregnant: minimal. MDT management Ascertain subtype of vWD pre-pregnancy and whether the disease responds to DDAVP. Avoid aspirin and NSAIDs.

Answer 403

Manifestations of a similar mechanism of microvascular platelet aggregations Thrombocytopenia - consumption of platelets at sites of endothelial injury and microangiopathic haemolytic anaemia TTP: extensive and systemic - often CNS involvement HUS: less extensive, predominantly renal invovlement BOTH RARE in pregnancy and puerperium but exacerbated by pregnancy Most commonly seen PP - Microangiopathic haemolytic anaemia: anaemia that results from damage to red cells following the occlusion of arterioles and capillaries because of platelet aggregation. Excessive production of vWF --> aggregation!!!! OR TTP - deficiency of specific vWF cleaving protease (familial) or there is an inhibitor of this protease (ADAMSTS-13) (non familial) - Schistocytes present on blood film - Sometimes bili and LDH raised - Thrombocytopenia - Clotting times and fibrinogen are normal. Consumptive coagulopathy (DIC) rare. - FEver - Neurological manifestations: drowsy, irritable, seizures, coma, fever - AKI HYPERTENSION not common!!!!!! Usually severe and associated with increased morbidity and mortality Management - Doesn't affect fetus - No evidence delivery affects course - Differentiate from HELLP and PET - FFP and plasmapheresis to limit vascular injury and improve prognosis - Supportive therapy for AKI and cerebral involvement - don't give platelet transfusions

Answer 404

Age Oestrogen deficiency: affects vaginal and periurethral collagen metabolism Pregnancy - 4 fold increase 1 pregnancy - 11 fold with ≥4 pregnancies Obesity and chronic increase in intrabdominal pressures Neuromuscular conditions: spina bifida, muscular dystrophy Genetic connective tissue disorders e.g. Marfans, Ehlers Danlos

Answer 405

1. Ligaments: cardinal, uterosacral. At apex 2. Muscular support upon which the vagina sits on - mostly levator ani 3. Angle of vagina in the pelvic floor

Answer 406

Puborectalis Pubococcygeus Illeococcygeus

Answer 407

Level 1: endopelvic fascia condenses to form cardinal ligament, uterosacral ligament. Failure = apical prolapse Level 2: endopelvic fascia condenses at arcus tendinus laterally and continuous with cardinal and uterosacral ligaments apically. Failure = anterior wall prolapse or lateral wall prolapse (Also pubo-cervical fascia is lateral to ATFP which connects cervix to posteiror pubic bone) (Also puburethrall ligament goes between posterior pubic bone to middle third of urethra and bladder to maintain bladder neck elevation) Level 3: endopelvic fascia continuous with perineal body posteriorly, perineal membrane anteriorly and the superficial and deep perineal muscles. Supports the distal 1/3 of the vagina and the urethra. Failure = urethral hypermobiliity, SUI and rectocele. (rectovaginal septum between vagina and rectum, pararectal fascia between rectovaginal septum and rectum, also posteiror to rectum (2 leafs) - pararectal fascia attaches to uterosacrals, perineal body and levator ani fascia. Failure in these two = rectocele)

Answer 408

stage 0 = no prolapse stage 1 = prolapse demonstrated but >1cm above hymen stage 2 = Between 1cm above and 1cm below hymen stage 3 = >1cm below hymen stage 4 = complete vaginal eversion

Answer 409

Aa - -3cm to +3cm. Anterior vaginal wall, 3cm from hymen Ba - -3cm to +tvl - rest of portion of anteiror wall above point Aa C - leading edge of cervix- length (of dependent position) gh - genital hiatus measurement anterior to posterior pb measurement anterior to posterior tvl = greastest length when returned to normal position Ap = -3cm to +3cm. Posterior vaginal wall point 3cm from hymen Bp = -3cm to +tvl. Posterior vaginal wall point - most distal dependent position of any part of upper posterior vaginal wall above point Ap and below point D D - posterior fornix

Answer 410

POPPY: PFMT one on one sessions vs leaflet : improved POPQ scores, self reported improvement Hagan et al Lancet: one on one PFMT + pilates, + visual aid vs leaflet. Significnatly improved POPQ scores, intervention sought less. QoL didn't differ and bladder and bowel symptoms didnt differ Cochrane: significant imporvement in prolapse symptoms, and clinical stage improved bu tPOPQ scores not improved.

Answer 411

``` 2020 Four studies Pessary vs no treatment: self reported improvement but low evidence Pessary vs PFMT: uncertain effect Combined: best ```

Answer 412

``` Short vagina Stage IV prolapse Incorrect choice i.e. needs space occupying Widened gh or levator avulsion Incorrect size ```

Answer 413

Restore anatomy and relieve symptoms Improve bladder or bowel function Maintain vaginal length and capacity for sexual function

Answer 414

Anterior colporraphy - 70-90% chance of success. ??40% risk recurrence Paravaginal repair Mesh repair - 11% risk mesh erosion / exposure, fistulae, scarring / stricture, pelvic pain at rest, dyspareunia.

Answer 415

Benefits: >90% successful. Completed vaginally, less invasive Risks: pudendal neurovascular bundle injury (go 1.5-2cm medial to spine), dyspareunia, cystocele (vagina pulled horizontally so increased intraabdominal pressure to anteiror wall), recurrence, sexual dysfunction, buttock pain, partial ureteral obstruction, recurrence 16%

Answer 416

Can be done vaginally, laparoscopically or abdominally Can be done at time of hysterectomy Stitch vault bilaterally to uterosacrals 80-90% chance of success Risks - Ureteric injury 1-10% - Bladder infection - Dyspareunia - Buttock pain - Infection, bleeding etc OPTIMAL trial: no difference in outcomes between SSF anf uterosacral ligation

Answer 417

Gold standard Uses mesh to suspend the vault or uterus to the sacral promontory. Sacral promontory is exposed by dissecting the peritoneum and clearing th eperiosteum of connective tissue. 2 or 3 non absorbable sutures are placed through the periosteum. Vaingal vault identified and bladder dissected off anaterior wall. 3 rows of sutures are placed as far down the posterior wall as possible and 2 rows anteriorly. All sutures are connected to the mesh. Success 90-98% Complications: bleeding, rectal trauma, ileus, mesh erosion (3%), occult SUI, sacral osteomyleitis Decreased dyspareunia compared to SSF Recurrence at 5 years <10%

Answer 418

``` More recurrence More awareness of prolapse More dysapreunia More repeat surgery More SUI post op ```

Answer 419

- Low hydrostatic pressure with filling - High compliance secondary to distensibility - Intrabdominal pressure increasing causes an increase in urethra before bladder - Rich blood supply and secretions around urethra (under oestrogen) to maintain closure - muscles enveloping urethrovesical junction (intrinsic (sphincter and smooth muscle) Pudendal nerve innervates urethral sphincter (Failure of the striated, or smooth msucel pshincter function, mucosal seal function or pudendal nerve innervation --> SUI (intrinsic sphincter deficiency). ``` Urethra supported by anterior vaginal wall. extrinsic sphincter (striated muscles of pelvic floor) and urethral support (anterior vaignal wall, pubocervical fascia is attached to ATFP and this is attached to pubococcygeus - when contracts elevates urethra and pressure inside urethra is higher than in bladder. With rising intradbominal pressure, the urethra is pressed downwards becasue attached laterally --> high pressure in urethra > bladder Failure of the mechanism can cause SUI - urethral hypermobility 2 condesations of hte endopelvic fascia connecting the urethra to the pubic bone - pubourethral ligaments (anterior and posterior) also support the urethra. elongation of these --> SUI ```

Answer 420

``` Funcitonal Neurological Metabolic Psychiatric Surgical e.g. fistulas ```

Answer 421

15 - 64: 30% >60y = 40% <60: stress > mixed > urge >60: Urge > mixed > stress

Answer 422

Bladder distension --> sympathetic outflow via hypogastric nerve -> stimulated pudendal outflow --> contracts ext urethral sphincter Hypogastric nerve contracts internal urethral sphincter and urethral smooth muscle and inhibits detrusor muscle contraction

Answer 423

Bladder contraction stimulates parasympathetic outflow via pelvic nerve to continue contracting detrusor muscle. Parasympathetic system inhibits sympathetic outflow to detrusor, internal urethral sphincter and urethral smooth muscle --> relaxation. Initiation: PSNS S2-4 --> hypogastric nerve --> acetylcholine --> M2, M4 muscarinic receptors --> detrusor contraction) Inhibits pudendal flow to urethral outlet Voiding: Rising intravesical pressure and falling urethral pressures = urine flow and bladder emptying Detrusor overactivity and UUI results from disruption at one of these levels (Storage, initiaiton, voiding)

Answer 424

``` Overactive bladder - dry or wet SUI Overflow incontinence Fistula Urethral diverticulum ```

Answer 425

Uroflowmetry: how the patient passes urine - Voids in commode: measures volume and flow rate (max flow rate should be minimum 15mL / sec - in a bell curve and maximum 40m/sec (if more possible outflow obstruction). If a flat curve with a low qmax = possible obstruction or detrusor hypoactivity. Measure residual Filling cystometry: how the bladder reacts to filling. Assess storage capabilities. - Filling and pressure catheter is inserted into bladder and pressure catheter into vagina or rectum. - Post void residual is measured - Bladder is filled - Detrusor pressure = intravesical pressure - abdominal pressure. Shouldn't increase during filling. DO = detrusor pressure rise in absence of abdominal pressure rise - Graph is generated - During filling phase record first sensation, first desire to void (150-200mL = normal), strong desire (>400mL) (+urgency or pain) - Bladder filled 50mL / min to 500mL or bladder capacity - Assessing for detrusor overactivity: tap run or hands into cold water - Cough etc: assess for SUI Voiding cystometry: greater details of pressure generated - Patient voids and pressure and flow are measured - Detrusor pressure should increase but <50cmH20 for a peak flow rate of <15mL/s - Slow flow: ?obstruction (cystocele), detrusor hypocontractility - Post void residual calculated - normal is <50 - 100mL (Videocystourethrography - combines routine cystometry with contrast media as filling fluid with radiological assessment of bladder and urethra - for complicated lower urinary tract dysfunction.

Answer 426

Australia: everyone having SUI procedure ``` Refractory urge urinary incontinence Awaiting SUI procedure ?? Mixed incontinence Stage 3-4 prolapse awaiting surgery Previous SUI procedure completed voiding dysfunction ``` NICE: no evidence to support the use of urodynamic testing prior to conservative treatemnt, nor to support its use in women with pure SUI, pre surgery. They recommend multichannel cystometry before surgery in women in whom DO is suspected when there has been previous SUI surgery or anterior wall prolapse or when symptoms suggest voiding dysfunction

Answer 427

1. Oestrogen 2. Antimuscuraninc - M2 , 3, 4 receptors in detrusor and bladder mucosa. Antimuscuranic mostly works in filling phase to increase capacity and decrease urgency SE: constipation, urinary retention, exacerbation acute angle glaucoma, dry mouth, blurry eyes, arrythmia / tachycardia, dyspepsia, dry mouth, dizziness, somnolence, impaired memory - Oxybutynin: 5mg TDS - Solifenacin 5mg OD (less SE) Beta 3 agonists in studies Desmopressin at night to prevent nocturia

Answer 428

ALWAYS do urodynamics first Aim: increase bladder capacity or modify innervation / contractility of detrusor muscle or bypass the lower urinary tract. Women will need to be prepared to self catheterize as voiding difficulty is common 1. Botox: stops release of neurotransmitters from nerves - effects sensory and motor pathways. Day procedure. 30% dry rate. Lasts 6-9 months 5-10% risk retention. Multiple injections safe and effective. Day case 2. Percutaneous tibial nerve stimulation: tibial nerve originates in L4 - S3 - stimulate tibial nerve with tens weekly treatment for 12/52 and then a maintenance phase. Decreases OAB 54% vs sham treatment 21% 3. Sacral neuromodulation: stimulation of sympathetic inhibiton nerve pathways. Batteries last 8 years. 1 stage lead inserted and must show benefit and then palce permanent battery. Complications: lead migration, pain at stimulation site, decreased efficacy over time, vaginal pain. 70% improvement.

Answer 429

Duloxetine: SNRI. Increases pudendal nerve activity - increases urethral sphincter closure. Not avialble in NZ NICE only recommends if patient declines surgery

Answer 430

Mesh mid urethral sling - Retropubic - Transobturator (No difference in short term subjective cure rates cochrane 2017. Longer FU: retropubic better. No difference in urinary retention, LUTS, infection Aim for transobturator was to avoid bladder and bowel injury Cure rates 85-90% at 1 year and similar long term. 1% erosion rates. Always treat OAB symptoms prior to procedure Pubovaginal (fascial) sling - Fascia lata - Rectus sheath Burch colposuspension Urethral bulking (50% success) Urinary retention Burch > pubovaginal sling > MUS > bulking

Answer 431

electrical energy --> heat (high current, low voltage) --> denaturing of collagen and elastin causing fusion of vessel wall, mechanical pressure causes coagulation of denatured proteins Vessels up to 7mm Measures impedance and then sends the correct amount of energy Gives feedback on when the tissue effect is complete and stops Ligasure - 5mm spread on 5mm, 1.8mm spread on 10mm. Seals up to 3 x SBP Enseal 1.8mm spread. Seals up to 7x SBP More reliable than ultrasonic for sealing tissues Risk of insulation failure, risk of altenrate path injury, produces smoke

Answer 432

Electrical energy --> mechanical energy (ultrasound waves) --> vibration 55,000 per second. This results in heat and caogulation by causing proteins to disorganise and form coagulum (rupture of hydrogen bonds, denature proteins) ACts at 50-100 degrees celcius Mechanical vibration causes bonds to stretch and break in tissue and results in cutting More tension = faster cutting and reduced coagulation ``` Pros Lower heat, less thermal spread Less smoke - gas plume only Instrument remains hot for longer Longer time to seal vessels Less reliable for vessels up to 7mm Increased tension = less haemostasis no charring / eschar ```

Answer 433

Vaporisation: cut not touching Dessication: cut or coag touching Fulguration coag not touching Coag: 6% on, 94% off - low current, high voltage Cutting: constatn low voltage.

Answer 434

Diathermy injury: freshen edges and traditional 2 layer closure with 3-0 PDS Sharp injury: invert mucosa, 1 layer interrupted 3-0 PDS Don't use non-absorbable, appose don't necrose, gentle squeeze test Twomey air test: 60mL syrunge full of air, tamponade promsimal part of bowel and 2-3 puffs of air into it.

Answer 435

Idenitfy extent of injury - if you can't see ureteric orifices, extend incision so you can 2-0 vicryl suture at apex with in 1 layer continuous if small defect, or 2 layers continuous and imbricating. Oppose don't necroses Cystoscopy and mild hydrodistension IDC for 10-14 days, cystogram prior to removal

Answer 436

``` Transection Resection Thermal Laceration Angulation Crush Ligation ``` 1/3 recognised intraoperatively. IV administration of indigocarmine (take 5-15 minutes to come through) Do cystoscope if suspected injury conservative management: minor crush injuries, needle injuries (provided integrity and viability i.e. peristalsis, perfusion, no urine leaking Stenting: obstruction (more significant crush injuries or ligature injuries), small areas of thermal injuries Suturing and stent: laceration injuries Excision of the affected part and re-anastamosis - deep thermal injuries Re-anastamosis - transection or resection Upper 1/3: end to end reanastomosis: uretero-ureterostomy Middle 1/3: uretro-ureterostomy or trans-uretero-ureterostomy Lower 1/3: reimplantation of ureter into bladder i.e. uretero-neocystostomy Sometimes psoas hitch is used to get closure to ureter sometimes boari flap (cut a section out of bladder and fold it up into a tube

Answer 437

``` S2-4 Greater sciatic formaen Lesser sciatic foramen Ischioanal fossa (pudendal canal) Splits into 1. Inferior rectal --> EAS, perianal skin, lower anus 2. Perineal --> superficial (skin), deep (deep and superficial perineal muscles) 3. Dorsal nerve of clitoris ```

Answer 438

External iliac | Beneath lateral umbilical ligament and runs in rectus muscles so unable to transilluminate

Answer 439

1. Superior mesenteric artery: intestine from lower part of duodenum through to 2/3 of transverse colon 2. Ovarian / gonadal - travels over pelvic brim and through IP ligament 3. Inferior mesenteric: supplies colon from splenic flexure to rectum 4. Middle sacral: from posterior aspect of termination of aorta, braches supply posterior rectum 5. Bifurcation above sacrum into common iliac arteries

Answer 440

Inferior epigastric Deep circumflex iliac artery Then continues as femoral artery

Answer 441

Posterior -> 3 branches - Iliolumbar (I) - Lateral sacral (Like) - Superior gluteal (going) Pudendal (Places) (In) Inferior vesical (My) Middle rectal (Very) Vaginal (Own) Obturator (only lateral branch) Umbilical (Obliterated distally) and UTERINE (Underwear) (only branch that crosses over top of ureter) (Uterine vein lies posterior to the ureter) +inferior gluteal

Answer 442

``` Prevesical space (space of retzuis) Paravesical spaces - uterine artery separates from pararectal space Pararectal spaces - lateral to ureter - useful space to identify ureter and iliac vessels and safe ligation of internal iliac or uterine artery Rectovaginal spaces (POD) ```

Answer 443

Develop pararectal and paravesical spaces Avoid the posterior trunk! - Buttock claudication - Go 5cm from bifurcation of common into ext and int Traction on obliterated helps visualise uterine Ligation medial to lateral minimizes damage to ureter Ligation lateral to medial minimizes damage to external iliac vein Ligate x 2 with absorbable sutures

Answer 444

``` Cervix: parametrial --> ilio-obtruator --> pelvic LN Uterus: pelvis --> paraaortic nodes Ovaries: para aortic nodes Vagina - Lower third: inguinal Upper third: similar to cervix ```

Answer 445

Exits kidney, descends retroperitoneally along psoas, enters pelvic brim by crossing over common iliac bifurcation lateral to medial, runs anterior to anterior division of internal iliac, underneath the IP, along the medial leaf of broad ligament, then turns medially at level of ischial spine and runs under the uterine vessels and into the bladder in an inferomedial direction Average distance of ureter from the cervix is 2.2cm at the right and 1.8cm at the left

Answer 446

- When it runs under the IP with transection of the IP - When taking the uterosacrals - When taking the uterines - When reflecting the bladder (tunnel of Wertheim)

Answer 447

Intraop - Inspection and await vermiculation (80% will still vermiculate) - Cystoscopy: only excludes total obstruction. Doesn't exclude partial thermal injury, devascularisation. Also look for blood Post op - Flank / groin pain, fever, retroperitoneal fluid collection, ileus, fluid leakage from wound - 50% asymptomatic - Creatinine very insenstivie - Imaging: CT urogram (most preferred), renal ultrasound

Answer 448

1. Real or percieved risk of ovarian cancer 2. Real of perceived risk of CHD, osteoporotic fractures, depression 3. Plan for approach for surgery 4. Any contraindications for MHT Not very good evidence to guide clinicians Unlikely for risk to outweigh benefit >55y Nurses health study: decreased risk of breast and ovarian cancer, increased risk all cause mortality, CHD Other studies didn't show same results - RANZCOG recommends consideration to be given to bilateral salpingectomy at the time of hysterectomy for benign gynaecological disease and that risks and benefits be discussed with the patient . No effect on ovarian reserve

Answer 449

2005 O&G Magazine Parker ``` Observational study Aim: Does benefit outweigh risk for BSO at time of hysterectomy for benign disease Inclusion 40-80y 4 groups - Oophorectomy + E - Oophorectomy - E - Conservation + E - Conservation - E ``` Risks balanced at age 65 Overall results: increased mortality by age 80 secondary to CHD and hip # Death 62% vs 54% with oophorectomy and no E replacement, compared to no oophorectomy and no E

Answer 450

Compared vaginal hysterectomy, TAH, TLH, robotic Vaginal hysterectomy best - Faster return to normal activities - Fewer febrile episodes TLH better than TAH - Faster return to activities - Fewer febrile episodes - Fewer abdominal and wound infections - Longer operating time Vag hyst better than TLH - Less urinary tract injuries Robotic - no advantages in this population

Answer 451

1: simple diagnostic endoscopic procedures 2: simple operative endoscopic procedures e.g. mirena retrieval, salpingectomy 3: More complex endoscopic procedures - Polyp resection - Excision stage 2 endometriosis - Oophorectomy without complexity - LAVH - Cystectomy 4: Advanced laparoscopy - TLH without complexity - LAVH with complexity - Adhesiolysis - SO with complexity - Stage 3 endo resection 5: AGES fellowship. - Endoscopic suturing - TLH with complexity e.g. fibroids, previous surgeries, adhesions, endo, burch colposuspension, myomectomy, stage 4 endo 6: Complex laparoscopic surgery 6B: benign gynae - extensive endo resection 6U: complex urogynae procedures 6R: complex reporductive procedures 6O: oncology procedures

Answer 452

<1% <0.5% serious 50% at time of entry

Answer 453

Fibrin deposition on surfaces resulting in fibrinous bridges Much worse if inflammation and ischaemia Much worse if bacteria, faeces, lots of sutures, powders etc. Cytokines, macrophages, histamine - all recruit more fibrin deposition Minimsation 1. Meticulous surgical tchnique and injury minimisation - gentle handling of tissue - Wash out afterwards - Meticulous haemostasis - laparoscopy over laparotomy 2. Adhesions barriers - Physical barrier between surfaces for a minimum of 72h - Solid: e.g. gortex, cellulose - Liquid (gels): PEG based liqud precursor, hyaluronic acid 3. Corticosteroids - meta-analysis minimal benefit 4. Oophorpexy Cochrane review 2015: insufficient evidence to draw any conclusions about the effectiveness and safety of anti-adhesion agents in gynaecological surgery, due to lack of data on pelvic pain, fertility outcomes, quality of life or safety.

Answer 454

Neuropraxia: compression - weeks to months Axontmesis: damage to axon with severe compression - months Neurotmesis: complete transection with damage to schwann cells - may never improve

Answer 455

Femoral: usually compression or abnormal positioning of leg (overly flexed, externally rotated, abducted - stretches). causes loss of hip flexion, knee extension, adduction Iliohypogastric and ilioinguinal - Transected at time of pfannenstiel incision if go past edge of rectus muscles or entrapped in suture - Sensory loss only - Iliohypogastric - skin of gluteal region - Ilioinguinal - labia majora, inner thigh Sharp burning pain Genitofemoral - Injured in pelvic side wall dissection as just lateral to external iliac vein - Causes loss of sensation / pain in labia majora, mons Lateral cutanoeus nerve of the thigh Compression with retractors Sensory loss anterior and postero-lateral thigh Obturator nerve L2-4 converges behind psoas and runs over pelvic brim behind common iliacs - Injured in TOT - Retroperitoneal surgery - Causes failure of adduction of thigh and sensory loss medial thigh Sciatic nerve and common peroneal nerve injured if hips overflexed or knees positioned abnormally Sciatic nerve: hip extension lost, sensory impairment below knee Peroneal: foot drop, calf and dorsum of foot loss of sensation Pudendal nerve - SSF - Pain over perineum, clitoris, gluteal region - Sexual dysfunction Brachial plexus Stretch injuries Hyperabduction of arm causes injury Erbs palsy

Answer 456

71000 women in 5 x RCTs Formal fetal movement counting Looked at perinatal mortality, morbidity, maternal anxiety, pregnancy intervention Not enough evidence to recommend

Answer 457

Large wedge - cluster RCT in UK and Ireland Introduced a FM awareness and timely delivery campaign to see if it reduced rates of stillbirth - E learning package for clinicians, leaflet for women and standardised management protocol for RFM from 24/40 including CTG within 2 hours of presentation, measurement of liqour volume wtihin 12h and then growth scan next working day, planned birth at 37/40 if any abnormal results. Primary outcome: stillbirth No difference 2018 Lancet

Answer 458

``` Aus and NZ BMJ 2018 Wedge-cluster RCT Intervention introduced over time App to raise awareness of FM with mothers Education program for clinicians Primary outcome: stillbirth <28/40 Results: no difference Low uptake of intervention ```

Answer 459

9/1000 Aus NZ 11/1000 Higher rates in indigenous population! Maori, pacifica, indian torres strait islander and aboriginal twice as high

Answer 460

Deaths after 20/40 or >400g and gestation unknown up until 7 days Perinatal related mortality up until 28 days post birth Early neonatal death first 7 days Late neonatal death 7 - 28/7

Answer 461

``` Previous stillbirth ETHNICITY Previous FGR baby Current FGR baby >35y or <20y Pre-existing diabetes APH Overweight and obesity Smoking (1.4x), drugs Primiparity and grand multiparity Low socioeconomic status Hypertension Multiple pregnancy 4 x higher GA at birth extremely preterm or >41/40 No antenatal care ``` 20-30% of these can be avoided with better care!!

Answer 462

placental dysfunction | PTL or PPROM

Answer 463

Spontaneous preterm birth 33.8% Congenital abnormalities 22% APH 15% Unknown 20-30% Overall perinatal mortality most common cause of death is congenital abnormalities becasue includes TOPs

Answer 464

``` 37 0.7 39 1.4 40 2.4 41 3.8 42 4.8 43 5.8 ```

Answer 465

Anti-cardiolipin Lupus anticoagulant Anti-B2 - glycoprotein 1 antibodies

Answer 466

Full: review of notes, full placental cytology, genetics and histopathology. External, radiological, dissection, organ evaluation, genetics, microbiology Limited: organ specific - may have incision Minimally invasive: e.g. laparoscopic sampling Non invasive: imaging, skin or needle biopsies, photos, placental examinations / histology Stepwise

Answer 467

Diagnosis - Privacy - Support - USS: 4 chamber view of heart, no movements, evidence of hydrops, maceration, skin oedema, abruption, skull collapse with overlapping Acknowledge parenthood: momentos, skin to skin Enable them to see / touch baby: prepare for appearance of baby Delivery - May have expectant management (85% labour within 3 weeks) - >48h is associated with increased medical complications (DIC), higher maternal anxiety, PM may be of reduced value, baby appearance may deteriorate Develop a birth plan - recommend VB, 90% achieve this within 24h, quicker recovery, lower risk for next pregnancy Unscarred uterus: Mife / miso or mechanical - Combination reduces time to delivery 14-28 weeks - Adjust miso dose depending on gestation (myometrial response varies and uterine rupture risk) Scarred uterus: discuss risks: mife okay, miso okay at lower dose of single LUSCS but not without risks. Oxy augmentation okay RANZCOG says Miso okay if use lower doses and caution but not if live doses NICE says not for miso CS if imminent delivery required Routine Abx not required unless signs of infection Analgesia Postnatal care - Wounds - Lochia - Lactation: cabergoline can be given but contraindicated with HTN or PET - Contraception - VTE risk - IUFD is not a risk factor Social work / cultural supports - financial, accomodation, certificates Psychological support Burial / cremation information Consultant to fill out death certificate Seek advice from coroner if any doubts - must be informed if sudden unexpected neonatal death. - Scene review, full autopsy, genetic metabolic screen Notify GP and other relevant care providers, cancel future appt Review case ASAP in audit meeting - assign cause of death (aingle factor with up to 2 assoicated), review relevant factors into case, have information for parents avaible Follow up meeting within 12 weeks - Cause - Risk of recurrence - Measures in future pregnancy - Document plan DIC risk 10% <4/52 - twice weekly coag surveillance 30% >4 weeks

Answer 468

SAFER baby bundle - Support smoking cessation (4-7% of SB would be prevented with smoking cessation) - Improved IUGR detection (risk assessment early pregnancy, growth surveillance if high risk factors) - Increased awareness and care for reduced FM - Encourage side sleeping (from 28/40, supine sleep position is an independent risk factor for stillbirth. - Improve decision making around timing of birth planning according to risk factors for stillbirth

Answer 469

``` REfer to obstetric clinic address modifiable risk factors: smoking, BMI, medical conditions Supplementation MSS FAS GDM screen Aspirin / ca if IUGR or PET serial growth scans if associated with IUGR (maternal reassurance) psychological support birth at maternity unit schedule birth ~39/40 or sooner if occured at different gestation / other RF vigilance for PND ```

Answer 470

Clinical syndrome defined by abnormal neurological function within the first week of life if born after 35 weeks. Involves Difficulty initiating respiration Abnormal tone and reflexes Subnormal level of consciousness / seizures

Answer 471

``` Severe = 60% Mild = 2% ```

Answer 472

``` HIE - if concern re hypoxic indication, cooling should be initiated for moderate to severe NE, for 72h. Reduces risk of long term neurological morbidity. Reduces second hit of apoptosis to damaged cells. Aim within 6h Metabolic disease Infection Drug exposure Neurological abnormality Stroke ```

Answer 473

1 / 2000 pregnancies Autoimmune condition causing synovitis, loss of articular cartilage and bone Symmetrical arthritis Symptoms: morning stiffness and pain Extra-articular symptoms / signs: inflammatory nodules under skin, scleritis (dry eyes), fatigue, vasculitis, anaemia Dx 1. Symmetrical joint involvement 2. RF and CCF 3. CRP and ESR 4. Time course Consider Secondary Sjrogens syndrome (lacrimal and salivary gland inflammation) - Anti-Ro and Anti-La antibodies Pregnancy effect on RA - 50% will improve - If worsens often secondary to stopping medications - 90% will have PP flare RA effect on pregnancy - Always check for Anti Ro and Anti La Ab - Refer obstetric physician and obstetric anaesthetist - Analgesics: paracetamol okay, NSAIDs contraindicated, and definitely contraindicated post 32/40 (renal impairment, oligohydramnios, closure of PDA) - Corticosteroids: continue (>5mg for >3/52 - stress dosing required - Immune modulators Azathioprine okay and okay for BF Sulfasalzine okay and okay for BF Mycophenalate teratogenic - switch to azathioprine Hydroxychlorquine okay and for BF cytotoxic drugs not okay e.g. cyclophosphamide, MTX (Folate antagonist - craniofacial, limb and CNS deformities). STOP all 3/12 prior TNFa antagonists: okay to use e.g. infliximab. but need to stop at various times in 3rd trimester depending on their half life becasue they cross the placenta and can cause immune supression in infant. Stop infliximab at 28/40. Avoid live vaccines

Answer 474

1:1000 Systemic connective tissue disease Flares and remissions Unknown cause but causes immune complex depositions in various areas causing arthritis (90%), nephritis, skin involvement (80%) such as malar rash and photosensitivity, vasculitis, neurological involvement (psychosis, seizures, chorea), haematological abnormalities (haemolytic anaemia, thrombocytopenia, leukopenia) 6% other AI conditions Labs - FBC - low Hb (low MCV, MCHC), low plt, low WCC, low neutrophils - CRP normal - ESR raised - Complement low in active disease - Renal function - ANA 96% of cases - titres don't change in disease activity - AntidsDNA - titres increase if disease active - Anti-sm titres Always check Anti-Ro and Anti La (30%) and Lupus anticoagulant (40%) as increase risk in pregnancy Pregnancy on SLE - 50% have flares as th2 mediated Skin and joints affected Renal disease can worsen (reversible) SLE on pregnancy - Miscarriage, stillbirth, PET, PTB, FGR - Worse if anticardiolipin or lupus anticoagulant present - Worse if renal nephritis Pre-pregnancy counselling - Check for - anti ro / la - APLS - anti ds DNA levels - C3, 4 levels - baseline proteinuria and renal function - BP Aim 6/12 from flare for conception If have lupus nephritis or APLS or vasculitis give aspirin Active disease or significant proteinuria give LMWH Growth scans Uterine artery dopplers UAPI from 24/40 If flare: symptoms, increased anti ds DNA, decreased complement, RBC / cellular casts in urine - Steroids - Hydroxychlorquine - Azathioprine Differentiation from PET difficult - viable deliver as normal - Non viable consider renal biopsy

Answer 475

This occurs if antibodies cross the placenta and bind to cytoplasmic ribonucleoproteins Anti Ro and Anti La <1% in population, but 30% in SLE, also in Sjrogens Causes a wide variety of symptoms but most common is neonatal cutaneous lupus (photosensitive rash over face mostly, disappears after months) - 5% risk of this if mother antiRo / La positive Most concerning is congenital heart block - 2% of fetuses - 20% mortality - Occurs in utero - AV heart block - inflammation and fibrosis of conducting system - Fetal heart circulation established by 12 weeks but CHB doesn't manifest until after 18 weeks - Pancarditis can occur - sometimes dexamethasone can halt progression, sometimes salbutamol can be given to increase HR, sometimes plasmaphoresis can work - 20% die in neonatal period, all should have pacemakers placed pre early teens to prevent sudden death If a previous sibling is affected then the risk is much higher Risk is decreased if taking hydrochlorquine

Answer 476

5% of obstetric population 30% of patients who have severe early onset FGR or PET C - coagulation defects L - livedo reticularis O - obstetric implications T - thrombocytopenia ``` Procoaulant state Inhibits angiogenesis Inhibits VEGF Inhibits appropriate trophoblast invasion and growth Promotes inflammatory state Complements binds trophoblasts ``` ``` Diagnosis Clinical symptoms Obstetric ≥3 miscarriages <10/40 ≥ 1 fetal death >10/40 1 x premature birth <34/40 secondary to PET or FGR ``` ``` Other VTE Stroke Heart valve disease Pulmonary hypertension Haemolytic anaemia Thrombocytopenia Livedo reticularis Cerebral involvement Leg ulcers ``` AND positive anticardiolipin IgG or IgM OR lupus anticoagulant OR antiB2glycoprotein 1 IgG or IgM on 2 occasions 12/52 apart Increases risk of - Miscarraige - PET - FGR - PTB - abruption - IUFD - thrombosis - worsneing thrombocytopenia Pre-pregnancy counselling - Aspirin recommended pre conception - Add LMWH at conception if recurrent miscarriages despite aspirin use, previous thrombosis (not currently on anticoagulation) - Add LMWH pre conception (>5/52) if on warfarin Check Ab AN care - MDT - FAS - Uterine artery dopplers - Growth scan from 28/40 - Baseline PET screen - Steroids and immunsupressive therapy not recommended PP - Thromboprophylaxis

Answer 477

1. Clitoris removed - partial or total 2. Clitoris partially or completely removed + labia minora, with or without majora 3. Narrowing of vaginal orifice with creation of covering seal by cutting and appositioning labia minor +/- majora with or without clitoris removal. Infibulation 4. Any other injury / piercing / needles etc

Answer 478

3% 6% primip 1.7% multips

Answer 479

``` Nullip - 6 x Asian EFW >4kg Shoulder dystocia Short perineum (<2.5cm) Forceps without episiotomy 6 x (22%) Forceps with episiotomy 1.3 (2.6%) Ventouse without episiotomy 9% Ventouse with epis 1.36% Previous OASIS 5 x risk OP position Prolonged second stage ```

Answer 480

I: Large RCTs with clear cut results II: Small RCTS with not so clear results III: Cohort and case control studies IV: Historical cohort or case control studies V: Case series, case studies with no control

Answer 481

Episiotomy: poor evidence for use in NVB Hands on approach: left hand on head, squeeze with right hand, no pushing with crowning - level 2 evidence Warm compresses Cochrane review RR 0.5 Perineal massage AN period and second stage: NNT = 15

Answer 482

mucosa: 3-0 vicryl , 75% remains 2/52 IAS: Interupted mattress 3-0 PDS, 70% 2/52, completely absorbed 6 months EAS 3-0 PDS 70% 2/52, completely absorbed 6 months - End to end vs overlap: no difference in dyspareunia, perineal pain, flatus incontinence at 12/12. Overlap significantly less anal incontinence at 12/12 but no difference at 36/12 Perineal muscles - 2-0 vicryl rapide: completely lost tensile strength at 14 days Perineal skin: continuous sutures = less dypareunia, less analgesia, less pain, less suture removal

Answer 483

3a / b = 22% 4th = 50% 5-7% 2 previous 9.5%

Answer 484

Parametrium, pelvic nodes, para-aortic nodes External iliac > obturator > parametrium > common iliac >pre sacral > para-aortic Risk of pelvic LN spread 1A1 0.6% 1A2: 7% Risk of para-aortic LN spread IVA 50%

Answer 485

Imaging or EUA / histopathology EUA - vaginal, rectal exam - assessment of size, spread LN: inguinal and supraclavicular Cystoscopy and proctoscopy can be used Pelvic USS CT CAP MRI - best for LN - controversy - may miss micrometastases PET scan Renal USS Sometimes fine needle biopsy of LN in areas with high HIV / TB Previously LN weren't involved in staging but they have a strong association with prognosis Currently ovarian involvement doesn't change the stage. <1% cases of SCC and 5% of other types of cervical cancer IN NZ staging typically involves preoperative MRI OR EUA with cystoscopy

Answer 486

Oestrogen stimulates increased fat in breast and for the lactiferous duct system to form Progesterone stimulates the lobules to increase (where milk produced) Progesterone decreases once baby is born which increases PRL and this stimulates milk production in the lobules Oxytocin secondary to suckling causes the myoepithelial cells in the lobules to contract and secrete milk down through lactiferous duct system Suckling also increases PRL Neuroendocrine reflex also secondary to crying, causes myoepithelial cells to contract

Answer 487

``` Major risk factors female age - 75% occur after menopause FH but >95% sporadic Genetics <1% Personal history: previous breast cancer or prelmalignant changes ``` ``` Minor risk factors - Oestrogen from subctuaneous fat, exogenous sources, early menstruation, late menopause, nullip EOTH / smoking RTX to chest or face Dense breasts ```

Answer 488

``` Histological - special type vs no special type Molecular - Luminal A - Luminal B - HER enriched - aggresive - Triple negative - aggressive TMN staging ```

Answer 489

``` Mammogram 45y - 69y 2 view mamogram o.4mSV radiation (CXR 0.1) 25% reduction in stage III-IV disease 30% reduction in mortality For every 2000 women screening per 10 year period 1 womens life will be prolonged, 10 will get falsely diagnosed with breast cancer ```

Answer 490

Clinic - history and exam Radiological - mammogram, USS +/- MRI (MRI if high risk features) Histological - core biopsy

Answer 491

Multimodal Breast conserving therapy: WLE with adjuvant radiotherapy (if margin negative same overall survival as mastectomy - 5% recurrence) Mastectomy - balance tumour size and breast volume e.g. small tumour large breast BCT, not large tumour small breast Contraindications to BCT: locally advanced, strong FH, patient preference, when adjuvatn RTX can't be given. Axillary: SNB or axillary dissection Neoadjuvant medical treatment - Herceptin - Chemo - Aromatase inhibitors

Answer 492

<10% of newly diagnosed breast cancers Suggestive FH - 3 or more relatives with breast or ovarian cancer - 2 relatives with with breast cancer and with one diagnosed <50y - 2 relative with breast cancer diagnosed <40y - Breast and ovarian cancer in same patient - Bilateral breast cancer - Male breast cancer - Ashkenazi Jew ancestry with breast cancer (BRCA) BRCA 1:400 - 600 Ashkenazi individuals risk is 1:40

Answer 493

Autosomal dominant mutation of BRCA1 or BRCA2 tumour supressor gene - Impairs DNA repair system - Associated with high risk features: young patients, bilateral breast cancer, Ashkenazi jew - Associated with ovarian cancer (40%), hepatobiliary malignancy, melanoma, colorectal cancer, prostate BRCA 1 80% lifetime risk breast cancer - 70% triple negative - poor prognosis - BRCA 2 - 50% lifetime risk of breast cancer - often resembles sporadic breast cancer / hormone receptor positive Both: 40% risk ovarian cancer (CDH1: gastric anc breast cancer) Refer genetic servic Regular self breast exam Regular imaging and clinical review from 25y or 10y prior to age of youngest diagnosis - 6 monthly USS or mammogram. Allows diagnosis at an early stage but no actual clear evicence of survical Risk reducing surgery - bilateral mastectomy and reconstruction - cochrane 2010: reduces risk but not to 0% - Prophylactic BSO - reduces mortality secondary to reduced ovarian cancer as well as breast cancer risk in postmenopausal women, and reduces all cause mortality. Recommend at age 35-40 or earlier once family complete

Answer 494

Breast cancer diagnosed in pregnancy or within 1 year postpartum <1% 2nd most common malignancy in pregnancy << cervical cancer

Answer 495

No - pregnancy associated with a reduced lifetime risk (younger age at pregnancy = better) Pregnancy itself doesn't worsen prognosis if matched for age and stage - BUT tends to occur in a younger population which often carriers features of worse prognosis - higher grade, ER -ve - May delay diagnosis - leading to worsened prognosis (increased breast size / density)

Answer 496

Triple assessment - History / exam - Imaging: USS recommended (younger patient, denser breasts, no radiation) +/- mammogram with fetal shielding. (o.4mrads in mammogram, 5 rads linked to fetal malformation). Don't use MRI - galolinium. If staging required: focus on major sites of mets (liver, lung bone), USS liver, CXR, MRI spine without contrast. - Biopsy

Answer 497

Benign: fibroadenoma, lobular hyperplasia, galactocele, abscess, lipoma, hamartoma, cystic disease, lactating adenoma Rare: breast cancer, rarely lymphoma, leukaemia, TB Lactation associated: lactating adenoma, fibroadenoma, galactocele

Answer 498

Multimodal NO RTX Surgery: shouldn't be delayed, undertake in any trimester Same principles as not pregnant However, RTX contraindicated and optimal timing of RTX is wihtin 3/12 of surgery so wouldn't recommend BCT if unable to do this SLN biopsy: radioisotope contraindicated Avoid immediate reconstruction as prolonged anaesthesia and suboptimal symmetrisation Chemotherapy: not in 1st trimester, okay in 2nd and third trimesters. Delivery should be at least 2-3 weeks following last chemo sessnion to allow for maternal bone marrow recovery and minimize issues with neutropenia No tamoxifen - craniofacial defects and urogenital abnormalities, not okay in breastfeeding Not herceptin in pregnancy or breastfeeding: oligo / anhydramnios

Answer 499

``` Atrophic endometrium (60-80%) Exogenous oestrogen 15% Polyp - endometrial or cervical 2-12% Endometrial hyperplasia 10% Endometrial cancer 10% Cervical cancer 1% ``` also vaginal trauma, anticoagulants, non gynae sites

Answer 500

96% sensitivity | 61% specificity

Answer 501

99.6% 81% Pipelle samples 50% of endometrium 96% NPV

Answer 502

Increased proliferation of irregular shaped and sized glands. Gland: stroma ratio increased with atypia: enlarged epithelial cells that are hyperchromatic with prominent nucleoli and an increased N:C ratio. MOST important prognositc factor for pregression to carcinoma

Answer 503

<40y 1.3% Postmenopausal 10% Age depdendent

Answer 504

Without atypia: 2% over 10 years Atypical hyperplasia: 30% 20 years. Endometrial cancer co-exists in 30-50% of atypical endometrial hyperplasias

Answer 505

2% progression to cancer over 10 years 90% regression rates 1. Stop exogenous oestrogen: stop MHT, stop tamoxifen, reduce weight 2. TVUSS to assess for oestrogen secreting tumour - granulosa cell tumour. if cyst test inhibin and oestradiol 3. Progestogens - Mirena first line as successful in 90-95% of cases - OR 6 x at 1 year for regression in comparison to oral progestogen - If declines mirena recommend oral progestogens: Provera 20mg/day, Norethisterone 10-15mg/day 4. sampling at 6 and 12 months. If regressed can discharge. Can stop progestogen treatment but would recommend continuing. 5. Hysterectomy if: - no regression despite treatment - progression to atypical hyperplasia or cancer - return of abnormality following progestogen treatment - non-compliance with medical treatment or sampling - persistent AUB 6. PM - include BSO, premenopausal - consider BSO

Answer 506

Post menopausal or perimenopausal: hyst and BSO Pre menopausal: hysterectomy and BS +/- O. If O can have MHT Fertility sparing - Mirena or high dose oral progestogens - 85% regression, 26% relapse, 26% live birth rate - Mirena in, sampling at 3 months and 6 months. Then 6-12 monthly until has hysterectomy - Recommend at least one negative sampling before trying to conceive - Obesity: less likely to regress - Involve GONC - Involve fertility specialist: assisted reproduction can be considered as live birth rate is higher and it may prevent relapse with women who are attempting natural conception - prevents prolonged interval with no progestogen treatment

Answer 507

Tamoxifen is the endcorine treatment of choice for patients with breast cancer that is ER positive. SERM with anti-oestrogen effects in the breast but oestrogenic effects in other tissues including blood (increased VTE) bone, and endometrium - Oestrogen like changes in vaginal epithelium - Stimulation of endometriosis - Stimulation of benign fibroids - Stimulation on endometrium: benign cystic hyperplasia, polyps, proliferation and endometrial hyperplasia. Endometrial adenocarcinoma in postmenopausal women on tamoxifen: RR 4.01 1.6% 5 years, 3% 5-14 years. Small risk in uterine sarcoma Can induce ovulation May be teratogenic 10-40% of women have abnormal uterine symptoms when taking tamoxifen. No benefit in routine screening or sampling. Only investigate with TVUSS and hysteroscopy and endometrial sampling if AUB Incidence 2-3/1000 Incidental finding of thickened endometrium: controversial. No bleeding no further investigation unless other risk factors (long duration, FH, hypertensive, obese) Likely stop tamoxifen if diagnosed with hyperplasia - discuss with oncologist Cochrane review: no change in risk with Mirena for endometrial hyperplasia or breast cancer recurrence. underpowered study Letrozole - stop oestrogen production from adipose tissue. Most useful in post menopausal women. Fewer serious side effects than tamoxifen. Doesn't cause uterine hyperplasia or cancers or blood clots. Can cause bone thinning, joint stiffness and pain

Answer 508

Older age Oestrogen related factors - Late menopause - Nulliparity - Obesity - Limited exercise - Exogenous oestrogen / Tamoxifen - Oestrogen secreting tumours - Polycytisc ovarian syndrome - T2D FH - Lynch syndrome - 40-60% risk of endometrial cancer. TLH BSO recommended age 40 Protective factors - COC - Smoking - Caffeine - Exercise

Answer 509

Patient factors - Age - Performance status - Obesity - Comorbidities Disease factors - Stage - Grade - Molecular profile - Lymph node involvement - LVSI - Type: non-endometrioid histology worse - Cervical stromal involvement Centre factors - Access to treatment

Answer 510

Applied to whether you test for Lynch syndrome 3 relatives with diagnosis of lynch assoicated cancer - CRC, endometrial, small bowel, ureter, renal pelvis - 1 relative must be first degree relative to the other two - 1 must be <50 - At least two successive generations must be affected

Answer 511

Pipelle Pros - less invasive, easier to do, no delay, NPV >99% if negative and TVUSS ET <4mm. Cons: However, otherwise misses 10% of cancers. No evidence local anaesthetic improves pain Hysteroscopy - Detects vast majority of cancers - Upgrades 15% of cases - If abnormal appearance to endometrium 70% chance of cancer on histology, if negative hysterosocpy 2.5% chance - Possible that the fluid pushes malignant cells out into peritoneal washings

Answer 512

type 1: 80-90%, endometrioid adenocarcinoma, oestrogen dependent, usually low grade, perimenopausal / postmenopausal, good prognosis, often precursor is endometrial hyperplasia, tumour usually expresses ER and PR ``` type 2: 10-20% Other types: clear cell and serous adenocarcinoma most common Not oestrogen dependent. Typically occur in small atrophic endometrium - precursor serous endometrial intraepithelial carcinoma Older women High grade Poor prognosis p53 mutations psomoma bodies ```

Answer 513

MRI abdo pelvis: best for assessing depth of invasion e.g. difference between 1a and 1b (Sometime USS and CXR if low grade disease) CXR for type 2 cancers because increased risk of spread CT CAP: For staging high risk disease (GRade 3) Ca125 sometimes used

Answer 514

Uterine-ovarian (IP) Parametrium Presacral The above collectively drain into - Internal iliac / hypogastrium - External iliac - Presacral - Para-aortic - Common iliac

Answer 515

Femme: multicentre RCT 1000 women. 43% regression for adenocarcinoma. 82% for hyperplasia

Answer 516

3-4 monthly for 2 years 6 monthly for 2 years Examine No smear needed Majority occur within 3 years - 33% mortality 50% local recurrence 20% distant recurrence Treat with RTX if havent had yet Sometimes progetogens or tamoxifen can be used sometimes chemo

Answer 517

POLE - excellent prognosis TP53: poor prognosis - treat with chemo MMR defieicnt group - intermediate prognosis (Lynch syndrome) NSMP: no specific molecular profile - intermediate prognosis

Answer 518

Poor prognosis High stage, high grade, LN spread Pre op: CXR - high risk pulmonary mets, whole body CT, endometrial sampling Treatment - Laparotomy, TAH< BSO, pelvic and / or para-aortic lymphadenectomy is indicated mainly in carcinosarcome, not in leiomyosarcoma RTX can help reduce local recurrence but no overall survival benefit Chemo- unhelpful

Answer 519

1-3% concomittant finding with CIN Treat with - Excision - deforming and can shorten vagina and cause dyspareunia but get histopathological diagnosis and rules out microinvasion - CTX - 5 flouracil - similar results. Less deforming - Immiquimod 5%: immune modulating: better for multifocal lesions. 50% clearance rate of HPV. similar results to laser - CO2 laser - Radiation - Major surgical procedures: partial vaginectomy, total vaginectomy, - Conservative surgical removal

Answer 520

``` Rare 10% of vaginal cancers are primary metastatic: cervix, vulva, breast, endometrium, trophoblast, ovary, lymphoma More common in PM women. Prevention with HPV vacc Confirm with biopsy Staging is clinical ``` Risks - Immunosupression - Smoking - LSIL / HSIL: 2-12% risk of progression. Usually asymptomatic Management: presents with bleeding or malodorous discharge. Complex treatment as rare REfer MDM Spread - Direct extension Lymphatic spread: upper vagina to pelvic LN (obturator, internal iliac, external iliac), lower vagina to inguinal and femoral nodes. Haematogenous spread: lung, liver, bone SCC 90% Adenocarinoma 10% Grade 1,2,3 Stage I: cancer in vagina II: Paravaginal tissues III: pelvic side walls, lower third of vagina, hydronephrosis, pelvic or groin LN IVA: bladder or rectum or outside of pelvis IVB: distant organs Treatment - Surgery if small lesion (rad hyst + vaginectomy and lymphadenectomy or radical WLE if lower vagina) Radiation: majority of cases this is treatment of choice: EBRT or brachytherapy. Prognosis affected by - tumour factors: stage, tumour volume, location outside the upper vagina, HPV statis - patient factors: age, reporductive status, sexual function, perofrmance status Vaginal melanoma - poor prognosis

Answer 521

Incidence 1.5 / 100,000 Mostly >90y 90% SCC Also bartholins gland ca, melanoma, BCC, sarcomas, pagets disease --> adenocarcinoma Two different pathways - Differentiated VIN - from lichen sclerosis normally. Risk of progression of dVIN to vulval cancer is 50% in 10y - usual type VIN - from HrHPV, 30% of vulvar SCC. Risk of progression from HSIL is 10-15% in untreated in 10y, 3% treated Also smoking, immunosupression predisposes HPV vaccinatio reduces vulvar condylomata by 60% and VAIN and VIN by 50%

Answer 522

Aims: relieve symptoms, prevent cancer progression, preseve normal vulvar anatomy and function Options 1. Excision - WLE gold standard. Aim for >1mm clear margin. Best for concern re invasion, (raised, ulcerative, irregular borders, previous VIN or vulva cancer, dVIN), unifocal, limited resection required, not involving urethra, anus or clitoris. 3-22% will have occult invasive disease in VIN 2. Ablative - CO2 laser - best in multifocal disease 3. Topical - Immiquimod - immune response modifier. 12-16 weeks 3-5x / week. Erythema to skin. 50% complete response, 25% partial response, recurrence 16% - Topical fluorouracil - chemical desquamation, high toxicities, poorly tolerated. decision to use is based on concern malignant transformaiton (as don't get histopathology), location (e.g. clitoris - don't want to excise), focality, performance status Follow up - uVIN: 10% risk progression 10y. recurrence 50% -dVIN: cancer 50% 6 monthly inspection / colposcopy

Answer 523

``` Inguinofemoral LN metastases - most important factor - 92% survival no nodes - 75% survival ipsilateral - 30% bilateral - 25% >2 nodes - 0% >6 nodes High stage High grade Depth of invasion (increases risk of nodal involvement) Age and performance status of patient ```

Answer 524

On labia majora Ill defined erythema and lichenification Atopic background Irritants: imidazoles, steroid creams (always use ointments), soap and body wash, lubricants, pads, waxing, sweat, semen, clothing (tight, bunching, g-strings) Management - Control, not cure - Avoid irritants - cool compresses - Soap subtitutes - Cool compresses - Mid potency steroid ointment e. g. methylprednisolone aceponate ointment (advantan fatty ointment)

Answer 525

Well demarcated glazed erythema. Not shiny like when on elbows / knees - just red Often no hyperkeratosis FH Look for psoriasis elsewhere Management - Control not cure - use until rash gone, start when returns - Good skin care - Mild or mid strength steroid ointments: hydrocortisone (mild), clobetasone (moderate)

Answer 526

Women >men Likely autoimmune basis Chronic T cell mediated inflammatory dermatosis Exact cause and pathogenesis unknown Often itches, burns, some aasymptomatic White atrophic epidermis, fissures, purpura Sclerotic, thickened dermis Permanent loss of architecture Affects vulva only Malignant potential 2% SCC. minimum annual exam required for life + self exam Exam - Patchy whitening in the interlabial sulci Partial covering of clitoris by fusion of clitoral hood Asymmetrical shrinkage of labia minora and fusion of labia minor to majora Scarring, agglutination dx - Biopsy and clinical - Consider autoimmune screen Treatment - Clobetasol (dermol) BD 1/12, OD 1/12 then maintenance Avoid irritants Potent topical steroids protective against VIN

Answer 527

T cell mediated chronic inflammatory disorder Attack of epihtelial basal cells and a cycle of cellular damage and repair also affects mouth Erosive LP most common Hypertrophic type Classic type See Wickhams striae Loss of labia minora, destruction of normal anatomy including clitoris, erosive edges Pain, acute agglutination of labia 10% overlap with LS Malignant transformation can occur Close FU essential Biopsies of any suspicious lesions

Answer 528

5-7% of invasive vulva cancers Rare (1/1mil women) More common older women Lania minora and clitoris most common places Poorer prognosis if melanoma on vulva in comparison to other places

Answer 529

``` Older patients Pruritis Eczema like appearance, well demarcated. Often multifocal Immunohistocehmistry Sometimes underlying invasive adenocarcinoma ```

Answer 530

Candia albicans most common (85%) Also candida glabrata, C parapsilosis, tropicalis, sacharomyces cerevisiae If not albican species need longer treatment Boric acid pessaries 600mg vainga 2/52 Pregnancy: imidazole instead of boric acid pessaries

Answer 531

<5% 4 or more episodes in one year ?cyclical pattern Need maintenance treatment - oral fluconazole favoured as less likely to cause a dermatitis

Answer 532

podophylin bd 3/7, 4/7 off - continue 4 weeks imiquimod liquid nitrogen surgery / laser

Answer 533

``` A: Vulvar pain cuased by a specific disorder - Infectious - Neoplastic - Neurologic - Trauma 0 Iatrogenic - Horomonal deficiencies ``` B: Vulvodynia: 3/12 pain with no identifiable casue - Localized - Generalized - Provoked - Spontaneous - Mixed Can have overlap with chornic pain conditions

Answer 534

``` 6-8% of women Higher incidence in younger women, then second menopausal peak Genetic vulnerability in chronic pain Psycho social: anxiety / depression Sleep quality Central sensitization Immune inflamamtory repsonse e.g. candidiasis Pelvic floor muscle overactivity Hormonal factors ``` Q tip test muscle spasms skin changes ``` Treatment - Pelvic floor physio +/- biofeedback and dilators - Local anasthetic gel e.g. lignocaine - TCAs, gabapentin, topical or oral Topical capsiacum Sexual and relationship counselling Nerve blocks Surgery - vestibuloectomy ```

Answer 535

TLH vs TAH on disease free survival among women with stage 1 endometrial cancer: RCT JAMA 2017 Janda et al Multicentre, multinational RCT 27 surgeons ITT analysis Aus, NZ, Hong Kong 350 TAH 400 TLH Pelvic lymphadenectomy performed in both groups unless not indicated - grade 1 ot 2 <50% invasion on frozen section, or not safe (morbidly obese) - 60% TAH, 40% TLH 3 monthly FU first 2 years then 6 monthly until 5 years Medical imaging it symptomatic Primary outcome: disease free survival (calculated as between surgery and recurrence or new primary cancer or death assessed at 4.5 years after randomization Secondary outcome: recurrence of endometrial cancer and overall survival Primary outcome the same - No differnece in recurrence - No diffrence in deaths - QoL difference significant at 4 weeks, 3 months, 6 months - Intraoperative adverse events similar, post op events less freuqent in TLH, costs lower for TLH

Answer 536

``` Looks at whetehr unilocular or multilocular, thin or thick walls, vascualrity (colour score), septations, solid components, size, papillary projections, ascites, peritoneal nodules etc. Gives score based on this ORADS1: normal ovary ORADS2 <1% risk malignancy ORADS3: 1-<10% malignancy ORADS4 10 - <50% risk malignancy ORADS5: >50% risk ``` Higher sensitivity rather than specificity in order to not miss ovarian cancers. Validated for a small number of woman in a paper published in 2022. ORADs is more precise than RMI and is more of a continuum, helps risk stratify better ``` Disadvantages: Requires highly skilled ultraonographer Doesn't take into account pre or post menopausal status Doesn't take into account Ca125 Over calls ```

Answer 537

Mature cystic teratoma: contain elements of - Ectodermal: skin, hair, follicles, sebaceous glands - Mesodermal: muscle, urinary - Endodermal: gut, lungs Serous and mucinous cystadenoma - epithelial tumour - Multilocular, thin walled cysts 5 - <20cm. - Serous more common than mucinous - Mucinous more likely to be unilateral, larger, multiloculated

Answer 538

≥2 relatives with ovarian cancer at any age (related to each other first degree) One with ovarian cacner and one with breast cancer <50y One with ovarian cancer and two with breast cancer <60y One with ovarian and breast cancer ≥3 with colon cancer or 2 with colon cancer and one with stomach, ovarian, endometrial, urinary tract, small bowel cancer in two generations. One <50y Carrier of BRCA1, 2, MMR genes

Answer 539

TVUSS RMI Ca125 - raised in epithelial tumours. Elevted in 50% of early stage disease. elevated in 80% of non-mucinous ovarian cancers. Non specific Ca19-9: elevated in 80% mucinous tumours, 27% serous CEA: 37 mucinous. Ca125 / CEA ratio <25 suggests krukenberg HE4 not available in NZ CT CAP only if high suspicion of malignant spread or very complex looking cyst Or MRI - but second line

Answer 540

- If RMI < 200 and Asymptomatic, unilateral, simple cysts <5cm - repeat scan in 4-6 months. if remain unchanged or reduce in size, with normal Ca125 can discharge. 50% will disappear - If RMI <200 and symptomatic, bilateral, complex, >5cm, non simple features, multilocular --> laparoscopic BSO - If RMI >200 - GONC MDM - If high suspicion - full staging procedures - If low suspicion - TAH BSO, omentectomy, peritoneal cytology under gynaecologist

Answer 541

1% incidence ``` Risks - Genetics (although majority sporadic) BRCA1 50% BRCA2 20% HNPCC 10% - Age - Oestrogen related factors --> nulliparity, infertility, obesity, HRT use - USe of perineal talc - endometriosis - Smoking ``` Protective factors - BSO - COC RR 0.7 - BF 0.7 - Sterilisation 0.7 - Has had children 0.7 - Hysterectomy 20% reduced risk Majority diagnosed at stage III or IV 75% 40% survival rate overall

Answer 542

Whether population screening reduced deaths secondary to ovarian cancer Published Lancet May 2021 RCT Looked at postmenopausal women, randomised to multimodal screening - Annual Ca125 --> TVUSS if normal (multimodal screening) - Annual TVUSS - No screening (1:1:2) Primary outcome: death secondary to ovarian or tubal cancer 200,000 women No difference in deaths (0.6%) Overall, MMS group were diagnosed at lower stage but didn't translate to lives saved, therefore population screening can't be recommended UKFOCSS also didn't show a better overall survival with screening - high risk women, annual screening, no difference in survival

Answer 543

Epithelial (70%) - High grade serous >70% - Mucinous <4% - Clear cell 10% - Endometrioid 10% - Low grade serous 4% Germ cell tumours 20% - Teratomas - Dysgerminomas - YS tumours - Embryonal tumours - Mixed germ cell - Choriocarcinoma Sex-cord stromal 10% - Granulosa - Sertoli leydig

Answer 544

High grade serous carcinoma - 70% - 80% present with high stage disease Peak age 45-65 <10% confined to ovary at time of diagnosis High level of genetic instability and are often associated with TP53 mutations and BRCA (10% have BRCA mutation) Smooth or friable surface papillae Microscopic to >20cm Cystic and multilocular with serous or bloody fluid and soft friable papillary excrescences Mets: firm nodules, often coalesce into large masses such as omental cake in up to 25% of cases 75% have STIC (SEEFIM protocol) ENDOMETRIOID CARCINOMA - 40-50yo - 10% - diagnosed at an ealier stage so much better prognosis assoicated with endo - incessant ovulation, endometriotic lesions around ovary associated with endometrial carcinoma in 20% of cases most common type assoicated with lynch syndrome CLEAR CELL 10% - More likely in perimenopausal patients 40-50yo - Presents at an early stage often - good prognosis. BUT if presents at a later stage then worse prognosis than serous or endometrioid as not as sensitive to chemotherapy Associated with endo Associated with lynch dynrome Large mass, usually thickwalled cyst with fleshy nodules MUCINOUS CARCINOMA 3% - late 40s to 50s but can present in young and old - most present with stage 1 disease - Lots are mets from GI tract - Most mucinous carcinomas are though to arise from borderlines - Can be very large. typically cystic or solid, unilateral, confined to ovary - if bialteral almost always from GI tract - GI immunophenotype: 75% have KRAS mutation. Also Tp53, HER2, cMYC LOW GRADE serous carcinoma <5% - Uncommon. Typically diagnosed at advanced stage, long term prognosis poor Slow growing, relativel insensitivty to platinum based CTX Often found with serous borderline component Carry KRAS and BRAF mutations

Answer 545

``` alopecia nausea vomiting neurotoxocity arthralgia hypersensitivity reaction nephrotoxicity neutropenia ```

Answer 546

``` Thrombocytopenia Nausea and vomiting Hypersensitivity reaction Nephrotoxicity Neutropenia ```

Answer 547

At completion of childbearing Or by age 40 for BRCA1 or 5y prior to sentinel family event By age 45 for BRCA 2 or 5y prior to sentinel family event Reduces ovarian cancer risk. 3% get primary peritoneal cancer Halves risk of breast cancer by 50% Cna do BSO or TLH BSO (eliminates EC risk, no P needed for MHT which increases risk of breast cancer, Treats DUB, large and more morbid procedure, loss of fertility options If on Tamoxifen increases risk for endometrial cancer

Answer 548

20% of benign and malignant ovarian tumours Malignant germ cell tumours 2-5% of all ovarian malignancies 80% are preadolescent malignant ovarian tumours Malignant GCTs arise from primordial germ cells derived from the emrbyonal gonad and are classified by the type of cell that is produced Increased in patients with gonadal dysgenesis, sexual immaturity and presence of an abnormal karyotype with multimodality treatment - surgery and chemo, most patients have an excellent prognosis and preservation of fertility is possible Any patient of childbearing age with a suspicious ovarian mass should have AFP, BHCG, Ca125 and LDH Adolescents and young adults should also have inhibin B and AMH to rule out sex cord stromal tumours Germ cell tumours - Undifferentiated --> dysgerminoma 45%. Produces LDH, sometimes HCG. Immature germ cells - Differentiated -- Whole blastocyst - Embryonal carcinoma <5% - RARE -- Embryo - teratomas 20-40% (immature and mature). From trilaminar disc (ectoderm, endoderm, mesoderm). Produce AFP and sometimes LDH -- YS - YS tumour 20% - produce AFP -- Trophoblast - choriocarcinoma <1% Mixed germ cell from blastocyst They grow rapidly so often present with stage 1A disease Bilateral in 10% 10-30yo Do USS and contrast enhanced MRI pelvis CT CA MRI brain if any disease above diaphragm ``` Adverse factors >45yo >stage 1 Incomplete surgical resection YS tumour ``` Managament - Surgery +/- chemo depending on stage - 1A: USO, omentectomy, washings, peritoneal sampling, contralteral ovary and LN assessment - laparotomy to prevent spillage. Risk of relapse low but if does occur easily salvaged with chemo. Frequent tumour markers and follow up until 10 years. Regular imaging - 1B: Aim USO and cystectomy. Case by case basis for chemo 1C: post op chemo - BEP Metastatic disease: chemotherapy primary treatment. platinum based chemo - BEP 0 bleomyin, etoposide, cisplatin 90% remission ``` SE chemo - N+V Fatigue Sore mouth Tinnitus and hearing loss Peripheral neuritis Nephrotoxicity myelosupression Pulmonary toxicity ``` Wait 2 years before next pregnancy

Answer 549

1-2% of malignant tumours are sex cord stromal Histology usually low grade, LN mets rare, prognosis good Average age 50y No ass with BRCA granulosa cells - adult granulosa cell tumour - malignant. excess oestrogen in <50% of patients. unilateral. endometrial hyperplasia 50%. virilization possible. Raised Inhibin, AMH, Ca125 theca cells - thecoma - benign, PM women, large, unilateral, solid. EXCESS estrogen - endometrial carcinoma in 25%. No tumour markers raised. TH and BSO leydig cells - leydig tumour fibroblasts - benign fibroma - PM women, unilateral Sertoli cell tumour: benign or malignant. 50% functional hormones - virilization, excess oestrogen Mixed - Sertoli leydig: benign or malignant. Second and third decade of life. large unilateral, solid. 1/3 patients have virilisation, 1/3 excess oestrogen AFP, inhibin Work up USs Bloods: total testosterone if virilization, estradiol, inhibin A and B, AFP, pipelle if AUb or thick ET ``` Management - Surgery - Surgical staging USO if fertility wishes and stage 1 disease - Sometimes give chemo ``` most diagnosed at early stage and low grade

Answer 550

3-15% breast, colon, stomach appendix, GI tract, pancrease, cervix

Answer 551

Surgical debulking Stage 1 or 2 disease with no residual disease - delay chemo until postpartum, surveillance in pregnancy stage 3 or 4 - TOP or delivery --> surgical cytoreduction followed by chemo OR - Biopsy --> NACT --> delivery --> treatment Carboplatin / paclitaxel okay

Answer 552

BRCA1 - 17q. Autosomal dominant. 40% risk ovarian cancer, 80% risk breast cancer BRCA2 13q - autosomal dominant. 20% risk ovarian cancer, 50% risk breast cancer Both are tumour supressor genes that play a role in DNA repair 1:300-800 Askenazi jews 1:40 Majority ov cancers high grade serous BRCA1 - most breast cancers triple negative, poor prognosis Other cancers: hepatobiliary, melanoma, CRC, prostate If known about BRCA - COC - 50% reduction - No recommendation for screning - RR BSO 40y 85-95% risk reduction. 3% will have a tubo-ovarian malignancy found. ?full staging following. Remove each side ovaries and tubes in separate bags in the event of occult cancer. SEE-FIM protocol - HRT in those who haven't had breast cancer. PROSE study 2002 - RRBSO reduced breast cancer by 53% if have surgery prior to menopause.

Answer 553

Autosomal dominant 3% of endometrial cancers CRC, endometrial cancer, ovarian cacner, stomach, renal, urinary, small bowel, brain, sebaceous tumours Occurs becasue of mutations in mismatch repair genes: MLH1, MSH2, MSH6, PMS2 Endo cancer lifetime risk 40% Lifetime ovarian cancer 10% - clear cell or endometrioid Prophylactic RR TH BSO once complete childbearing / age 40y, or 5y prior to sentinel family cancer event. - doesn't eliminate risk - low dose oestrogen only HRT can be used until menopause following. - Some recommend COC or progesterone to reduce endometrial cancer risk - Some recommend aspirin??? - Refer to colorectal for ongoin screening, consdier urology referral - Colonscopy every 1-2y from age 25y, or 5 years prior to earliest CR ca in family ACOG recommends pipelles from 30-35 y every 1-2 y - Australian guidelines do not!! Studies that look at endometrial biopsy and TVUSS in women with Lynch don't see a survival benefit. definitely pipelle if abnormal bleeding

Answer 554

JAMA 2011 Does ovarian cancer population screening reduce mortality from ovarian cancer Baseline and annual TVUSS for 3 years Baseline and annual Ca125 for 5 years Initially included bimanual but then stopped Aged 55 to 74 Primary outcome: death from ovarian cancer - No change - No change in stage - 5% FP rate which resulted in overtreatment 68,000 women included Multicentre RCT

Answer 555

Atypical epithelial cells with slow growth, malignant potential, no stromal invasion In 10% of cases there are areas of microinvasion

Answer 556

60% of women dx <40y 95% 5 yr survival Serous: 45-60% - Usually bilateral - Large masses with papillary projections - Typical pattern 90%, micropapillary pattern 10% - 2% risk progression to low grade serous cancer - 70% dx stage one - Can get peritoneal implants 30% Mucinous 30-50% - More commonly larger, bilateral, complex or unilocular, intramural nodules, fine septa - Uncommon to have peritoneal implants - Commonly dx stage 1 - Intestinal type 90% - if bilateral consider primary gastrointestinal tumour. - Endocervical or mullerian type 10%. Bilateral in 40% of cases. Ass with endometriosis - Peritoneal implants uncommon Ca125 elevated in 50% Ca19-9 non specific but elevated in mucinous borderlines CEA mucinous borderline Same staging as ovarian cancer Treatment - Surgery: - can do frozen section to determine extent of procedure. Good sensitivity and excellent specificity. Risk of under diagnosing = 10%. Much higher chance of getting an inaccurate result if large mass - Otherwise recommend staging procedure: TH, BSO, peritoneal washings, omentectomy, resection of grossly visible mets - as well as sometimes multiple peritoneal biopsies. ALways look at all the surfaces same as ovarian cancer - Appendicectomy in cases of mucinous BOT sometimes done but recent evidence that this is very low yield (<1%) and increases risk of infection - Pelvic and paraaortic lymphadenectomy is not considered necessary - Fertility preserving surgery: worse prognosis recurrence 10-20%, compared to 5% depending on technique. USO +/- cystectomy + exploration of cavity etc. biopsy of contralteral ovary if abnormal. 23% recur if cystectomy. 11% USO, 5% BSO. Surveillance of other ovary every 6/12 + ca125 and uss If stage II or III and wishing further fertility: non invasive implants - conservative surgery okay if total resection. If invasive implants, majority will stay stable or disappear after primary tumour removed but still bad prognosis. Recurrence risk - High stage - Invasive implants - Incomplete surgery - Conservative surgery - More than 40y - Serous BOT - Papillary pattern - Microinvasion - Intracystic carcinoma - Extraovarian relapse - Size >15cm - Histological pattern with high numberof mitoses per field - elevated pre op ca125 doesn't respnod very well to chemo as slow growing

Answer 557

P - polyps A - adenomyosis L - leiomyoma M - malignancy or atypical hyperplasia ``` C - coagulopathies O - Ovulatory disorders E - endometrial disorders I - Iatrogenic N - not otherwise classified ```

Answer 558

Localised hyperplastic overgrowth of glands and stroma that form over the endometrium Possibly they los their apoptotic cell regulation and over-express oestrogen and progesterone receptors causing them to grow. Incidence increases from age 20, declines at menopause. 30% of women with AUB will have polyps Malignancy risk factors - Polyp >1cm - AUB - PMB - Surface irregularities: necrosis, vascular irregularities and whitish thickened areas Remove if postmenopausal, premenopausal and >1cm or symptomatic If <1cm and asymptomatic can offer surveillance instead

Answer 559

Presence of non-neoplastic endometrial glands and stroma in the myometrium - Asymmetrical myometrial thickening - Myometrial cysts - Hyperechoic areas in myometrium - Linear striations - fan shaped shadowing - Echogenic subendometrial lines and buds - Translesional vasculatirty - Irregular junction zones - Interrupted junction zones Risks factors: increasing parity, termination of pregnancy, uterine curettage, CS birth - all can disrupt the endo-myometrial junction causing infolding of endometrium into myometrium Increasing age = increasing oestrogen exposure = increased adenomyosis Tamoxifen Smoking protective Defined histologically - no USS or MRI defined criteria - presence of non neoplastic endometrial glands and stroma in myometrium, often associated with hypertrophy and hyperplasia surrounding the ectopic endometrial tissue MRI: diffuse junctional zone thickening, high intensity clefts. Better sensitivty and specifcity - but high cost Treatment: hysterectomy or Mirena (comparable effects)

Answer 560

Smooth muscle tumours of uterus-monoclonal incidence 70-80% Management First step - Hormonal - COC, Progetogens, Mirena, Short course GnRH Wishing to conceive - NSAIDs, TXA Second step: hysteroscopic myomectomy +/- endometrial resection / ablation +/- Mirena Or if wishing to conceive: hysteroscopic myomectomy, laparoscopic myomectomy Second step: minimally invasive uterus-conserving treatments - Uterine artery embolisation Magnetic resonance-guided focused ultrasonography Laparoscopic uterine aryeru occlusion Third step: hysterectomy +/- BSO or abdominal myomectomy

Answer 561

1. Exogenous sex steroids altering hormonal environment and causing unscheduled bleeding and breakthrough bleeding 2. Drugs that alter drug bioavailability by altering hepatic enzyme metabolism - anti-epileptic, anti TB drugs, - alters sex steroids circulting 3. Anticoagulants 4. TCAs and phenothiazines (e.g. prochlorperazine) - block dopamine receptors resulting in hyperprolactinaemia (Also traumatic perforation)

Answer 562

Length of cycle ≥24 - ≤38 Bleeding ≤8/7 Regularity - <7-9/7 variation in each cycle

Answer 563

Done under GA, sedation, regional Angiography catheter inserted directly into femoral artery and the contralateral uterine artery is then selectively catheterized Polyvinyl aclohol is mot commonly used Then the other side is done Vaginal and ovarian collaterals recovers the circulation to the remaining myometrium Takes 45mins 20 rads of ioninsing radiation Contraindications: active infection or malignancy Relative contraindications: submucosal myomas, pedunculated myomas, recent GnRHa, previous UAE, post menopausal status cochrane review compairson to other surgical interventions (myomectomy, hysterectomy) - No significant differnece in patient satisfaction in 2 or 5 years Similar intraprocedural complications No difference in short or long term major complications UAE had a shorter procedure, length of hopsitlaisation, time to resumption of normal activities UAE had an increased risk of short and long term minor complicatcations, number of unplanned reviews and readmission, surgical reintervetnion rate (OR 3.7 at 2 years, 6 at 5 years) No long term difference in POI (risk of this so difficult evidence to recommend prior to pregnancy or not) Possible myomectomy better for pregnancy rates - UAE probable decreases endometrium volume due to inadequate blood supply therefore affecting immplantation rates and contraction disturbance Recent meta-analysis: myomectomy better - less miscarraiges. once pregnant no difference in rates of bad outcomes EMMY trial: 20% hyst at 2y, 35% at 10y Minor complication rate 30-45% Always consider malignancy Patient must be willing to accept hysterctomy if complication Narrow stalked pedunculated and large intracavitary submucosal fibroids are at risk of detaching and significant sloughing into endometrial cavity, leading to cervical obstruction and occasionally sepsis. Major: 5%

Answer 564

Best: vaignal Second: abdominal Third laparoscopic From NICE guidelines 2007 TLH had most major perioperative complciations including vascualr injury, vaginal vault infection, UTI Abdominal: other febrile condition and wound infection

Answer 565

Common haematological cause of HMB vWF normally binds to Factor VIII and platelets to form platelet plug 1/100 peple 3 main types - Type 1: 60-80%. Low levels of vWF in their blood (20-50% of normal). Mild symptoms - Type 2: 15-30%. Normal levels byt doesn't work properly - mild to moderate symptoms - Type 3: 5-10% - very low levels or no vWF in their blood. Severe symptoms including bleeding into their joints or muscles Can give COC --> increases fibrinogen, prothrombin, factor VII , factor VIII and / or vWF Mirena is affective endometrial ablation vWF and desmopression acetate may be required for replacement

Answer 566

11% by age 44 80% attending pain clinics 50% attending fertility clinic 700,000 girls and women in Australia 176 million worldwide 10x risk if one first degree relative affected

Answer 567

Develop a network of endometriosis expertise Raise public awareness of endometriosis Treatment strategies for endometriosis Improve understanding of endometriosis through research

Answer 568

``` First degree relative with endometriosis (7x as likely) Shorter than normal menstrual cycle Longer than normal menstruation Low BMI Early menarche Nulliparity Mullerian abnormalities Out flow obstructions e.g. cervical stenosis, a transverse vaginal septum or an imperforate hymen Retroverted uterus ```

Answer 569

1. Retrograde menstruation - Adhesion and initation of lesions - Samson's theory - Can also deposit endometriotic deposits that are stem cells which implant and differentiate 2. Activation of misplaced endometrial cells left behind from the unusual differentiation and migration of Mullerian ducts during development - Embryonic remnant 3. Metaplasia - e.g. transformation of coelomic epithelium covering ovary 4. Genetic factors: 50% heritability. 9 regions identified. Mostly affect genes associated with cell proliferation, cell adhesion and angiogenesis 5. Environmental factors: inverse association with BMI, specific dietary factors, possibly exposure to endocrine disrupting chemical 6. Immunologicla factors: oxidative stress and inflammation and immunlogical changes that promote growth. Prevention of immune system to clear debris 7. Apoptosis dysfunction 8. Hormone driven: oestrogen mediated, resistance to progesterone changes

Answer 570

Pain discomfort or pressure percieved to be related to bladder assoicated with frequency and urgency Improves with voiding Negative MSU >6/12 Treatment - conservative measures: diet changes, stop smoking, stress management, analgesia, physiotherapy, some data on acupuncture, bladder training, support groups - pharmacological: anticholinergics, cimetidine, pentosan polysulfate - infiltrating medications: lidocaine, hyaluronic acid, botox (every 1 - 2 weeks for 6-8 weeks) surgical options: cystoscopic fulguration and laser treatment of hunner lesions. neuromodulation

Answer 571

psychosocial factors that increase the risk of development of chronic pain, drug misuse, disability Attitudes, beliefs, emotions, behaviours, famuly and work place factors

Answer 572

nociceptive: inflammation and tissue damage neuropathic: nerve injury Nociplastic: perceived long term pain with no organic stimuli Central sensitisation: hyper-excitability of the nervous system, usually including hyperalgesia (increased sensitivity to pain) and allodynia (painful perception of non painful stimuli

Answer 573

Allodynia / hyperalgesia Viscero-visceral hyperalgesia: IBS, PBS (shared neural pathways) Viscero - muscular / somatic hyperalgesia: myofascial pain or trigger points in abdominal wall or pelvic floor, which shares the same spinal segment as the sensitised viscera Other ass symptoms: headaches, fibromyalgia, fatigue, dizziness Small stimuli or assoications of stimuli can now set off pain patheays - wind up, eventually pain can occur even once there is no organic stimuli Contributors: biologicla factors, psychological factors, diet and exercise, environmental (poor sleep) Chornic overlapping pain syndromes: vulvodynia, temperomandibualr disorders, chronic fatigue, IBS, bladder pain syndrome, fibromyalgia, endometriosis, chornic migraine and tension headaches, chronic low back pain

Answer 574

1. Organ dysfunction: viscerovisceral cross sensitization: bladder, bowel, repoductive organs 2. MSK response to pain: most common muscle groups obturator internus and levator ani. better in fetal position. 75% of patients will have an MSK issue 3. Chronic sensitisation - hyperalgesia - allodynia (decreased pain threshold) - increased duration of pain after sitmulus - peripheral sensitisation 4. Psychological sequlae - Depression, anxiety, social isolation, poor sleep

Answer 575

peppermint oil - IBS TENS not useful Acupuncture - some evidence Diet: increase fish (omega - 3 fatty acids act as anti-inflammatories in endo and dysmenorrhoea by reducing the pro-inflammatory PGs ), veges, transfat exercise: inconclusive data - but decreases systemic levels of cytokines with anti-inflammatory and antioxidant properties

Answer 576

Pain: impairs normal sexual function Functional changes: altered tubal and endometrial function. Disordered tubal motility. Disordered myometrial contractions - impaired gamete transport and embryo implantation. Abberant gene expression and downregulation of progesterone receptors Pelvic environment / autoimmune dysfunction: altered levels of inflammatory cytokines, growth and angiogenic factors that may disrupt sperm activity, egg activity, fertilization and embryo transport Anatomical distortion: adhesions and distortions of pelvic anatomy, causing mechanical disruption to conception Ovarian reserve: reduced regardless of whether they Can do endometriosis fertility index score - looks at severity of tube and ovarian disease + age, + years infertile + reporductive history Lower the score = worse outcome

Answer 577

Stage I-II - excision improves pregnancy rates, probably also improves ART, don't do unless struggling with fertility Stage III-IV - excision improves natural pregnancy rates. No good data for ART Endometrioma - excision of capsule improves spontaneous pregnancy rates. Reduction in ovarian reserve. No evidence for improvement for ART. Consider surgery but in context of pain etc. Otherwise consider doing IVF without surgery Pregnancy outcomes: increase adverse outcomes inlcuding placenta praevia, PET, prematurity, APH, CS

Answer 578

Ovarian endometrioma: rupture, pelvic abscess after oocyte retrieval Peritoneal endo: haemoperitoneum, massive ascites GI: - Ileum: obstruction, perforation - Appendix: appendicitis, rupture - Caecum: obstruction, perforation - Recto-sigmoid - obstruction, perforation Urinary tract - Bladder: haematuria - Ureteric: obstruction, hydronephrosis, acute renal failure Pulmonary: catmenial pneumothorax, catamenial haemoptysis CNS - Intraspinal: cyclical cute low back pain - Sciatic nerve: cyclical sciatic pain

Answer 579

Increased coagulation factors - 8,9,10 Increased fibrinogen by 50% Venous stasis particularly in lower legs caused from vasodilation Concentrations of endogenous anticoagulants such as antithrombin and protein S fall Virchow's triad - Venous stasis - Endothelial damage - Hypercoaguability

Answer 580

point mutation on factor V which prevents its breakdown = hypercoaguable state Heterozygosity - 30-40% risk clot Homozygosity 50-60% lifetime risk of clot

Answer 581

Visualisation of the thrombosis Lack of compressibility of the vein Lack of distla distension of the vein with valsalva

Answer 582

V/Q scan recommended in all cases apart from if abnormal CXR and so higher risk of indeterminate result This is because it is more likely to have a determinate result V/Q technetium 99 is used so breast milk must be dumped for 12 hours if BF V/Q slightly higher risk of childhood cancer but less risk of maternal breast cancer - absolute risk very very small Total radiation to fetus with V/Q scan is very small and well below recommended total pregnancy maximal dose CTPA should be sued for haemodynamically unstable women as faster

Answer 583

Causes chonrodysplasia punctata (spots at end of bones), nasal hypoplasia, short proximal limbs, growth restriction 5% of cases highest risk between 5 and 12/40 Can be on Warfarin for conception but should stop at 4/40 increased risk miscarriage and SB 3rd trimester: increased risk of retroplacental clot and fetal ICH Need to use if have mechanical heart valve however

Answer 584

Doesn't cross placenta Heparin induced osteoporosis (2% UFH, 0.04% LMWH) thrombocytopenia (early vs late - late can be assoicated with a paradoxical thrombosis) UFH should do platelet count 2-3 daily from days 4-14 (Dabigatrin, rivaroxaban and apixaban not licensed for use in pregnancy)

Answer 585

Uncommon, 1/10.000 Headache, seizures, impaired consciousness, signs of raised ICP, vomiting, photophobia, hemiparesis, fever, leukocytosis, venous infarction, Pathogenesis: hypercoaguable PP state and possible trauma to endothelial lining of cerebral sinuses and veins during labour Obstrcution of venous structures --> increased cererbal pressure. BBB disruption --> vasogenic oedema, leakage of blood plasma into intersitital space, cerebral oedema, venous gaemorrhage due to capillary rupture Risk facors similar to DVT / PE Do CT venogram or MR venogram Management: hydration and anticoagulation, thrombophilia screen

Answer 586

Seizure in pregnancy Teratogenesis of AEDs - 5%, 10% with sodium valproate. dose dependent effect genetic risk of epilepsy to infant 10 x risk of maternal mortality

Answer 587

5% mother 10% sibling 15-20% both parents

Answer 588

Week 3 - gastrulation. Mesoderm --> sphlanchnic mesoderm --> heart. Progenitor heart cells from ectoderm down primitive streak Folds dorsally and caudally and laterally to fuse 2 x endothelial tubes and blood islands = day 20 heart pumping as a tube Right twist and folding over on itself - dextral looping week 4 - atrial septum, ventricular septum, endocardial cushion and septum between truncus ateriosus starts forming week 5: atria completely separated Aorta and pulmonary trunk completely separated Ventricles increasing in size week 6 and 7 - Ventricle separated - Arch formation from brachial arteries including PDA, subclavian etc week 8 - fully functioning and structurally the same as a neonates heart

Answer 589

Folate metabolism inhibition Toxic free radicals NTDs Orofacial abnormalites congenital heart defects Urinary tract and skeletal abnormalities Valproate - NTDs, congenital heart defects, urinary tract and skeeltal abnormaliteis AND valproate facial abnormalities: low set ears, broad nasal bridge, irregular teeth - fetal valproate syndrome

Answer 590

1. 5mg folic acid 12/52 prior and all way through pregnancy 2. Continue on carbamazepine, lamotrigine, levetiracetam 3. Counsel around risks with valproate - try to change or at least wean to <600mg - dose dependent effect and try and change to multiple daily doses to decrease peak effect 4. advise to relatives about recovery position if tonic clonic seizure, bathe only in shallow water 5. NT screening, detailed cardiac scan 6. Concentration of free drug falls - increased plasma volume, increased renal and hepatic clearance, decreased protein binding . Therefore need to measure drug levels if having seizures or if on lamotrigine. dose often needs to be increased 2-3 fold with lamotrigine 7. 18/40 anatomy scan - NTDs and cardiac defects. Biochemical screening with serum AFP when combined with USS - 94-100% detection of NTDs 8. Screen for mental health 9. Identify triggers and mitigate 10. Serial growth scans: growth restriction in WWE OR 1.26, 3.51 with AEDs. FROM 28/40 11. Education re pregnancy risks - WWE and no AEDs: Miscarriage, APH, HTN, IOL, CS, PTB, FGR, PPH. No differences in GDM - WWE with AEDs: IOL, FGR, PPH, NICU

Answer 591

1. Aim NVB 2. Tertiary hospital - increased risk seizures (1-2% of women in labour, 1-2% postpartum) - maternal hypoxia --> fetal hypoxia --> acidosis (hypertonus and maternal hypoxia) 3. Don't leave unattended in labour or first 24h 4. Continue regular AEDs in labour, consider IV if vomiting 5. Early epidural, IVL in labour 6. Avoid dehydration 7. No pethidine. Morphine okay 8. >5 minute siezure = abnormal. High risk for status epilepticus. - Left lateral - Oxygen, IV lorazepam (4mg over 2 minutes, repeat at 10 minutes), or PR diazepam 10-20mg, repeat at 15 minutes - Consier phenytoin if still no control - Tocolytic agents if uterine hypertonus 9. Water birth okay i seizure free for a long time and not taking AEDs and discussed with epilepsy specialist and hoist available

Answer 592

1. 3/7 PP highest risk time, continue AEDs 2. Vitamin K to prevent HDN - hepatic enzyme inducers include carbamazepine, phenytoin, phenobarbitol, primidone) 3. Neonatal withdrawal symptoms: lethargy, difficulty feeding, excessive sedation, inconsolable crying 4. encourgae breastfeeding: most AEDs excreted into milk but low fractions - Lamotrigine and phenobarbitone - higher amounts. DO not initiate lamotrigine in BF mothers but do continue on it with BF if already established. consider plasma testing on infant. close monitoring. Can BF prior to taking dose rather than afterwards 5. Downtitrate AED: lamotrigine quickly. Otherwise symptoms of toxicity 6. Mother should change nappies on the floor / bathe baby in shallow water or with supervision 7. Screen for depression!

Answer 593

hepatic enzyme inducing drugs: carbamazepine, phenytoin, phenobarbitol, primdone - Higher doses of oestrogen required - COC 50mcg or 2 x 30mcg pills. Still a risk of being ineffective POP also affected - need to take 2 Implants can be effected Depo: fine Mirena not affected Copper not affecetd Double dose of morning after pill Oestrogen can induce the metabolism of lamotrigine --> lowers drug levels so COC's not appropriate

Answer 594

``` chronic autoimmune demyleination syndrome affecting the CNS , not PNS 0.1% incidence 20-40y 15 x risk if first degree relative Relapsing and remitting course ``` Common symptoms - Optic neuritis - Sensory deficits - UMN deficits: spastic weakness of legs - Cerebellar involvement Less likely to present in pregnancy and less likely to relapse Risk of relapse rate increasing PP 25% of patients Overall long term outcomes not affected. Treatment in pregnancy - Vit D - Severe acute relapses treat with high dose steroids - Sometimes immune modulators given

Answer 595

Ab against AchR --> affects skeletal muscle - Ptosis, diplopia, dysphagia common features Ab can cross placenta and affect fetus - fetal arthrogyrposis - Contractures secondary to no movement - Poluyhydramnios secondary to affected swallowing - Mild cases: myopathies Skeletal muscle affected so pushing can be inadequate Transient neonatal MG: apparent in first 2/7 - hypotonia, difficult feeding, crying, floppy baby, resp issues. Improves over 2 days and with anticholinesterases Ass with thyroid disorders - measure thryoid function Continue anticholinesterases in pregnancy Continue immune supressants in pregnancy Obv stop mycophenolate and MTX Encourage monitoring of fetal movements Encourage NVB Plasmaphoresis and IVIG can be used for refractory cases Thymectomy delayed until after pregnancy 2/7 neonatal observation Avoid drugs that impair neuromuscualr transmission: gentamicin, propanolol, salbutamol, narcotics, MgSO4. MgSO4 can precipitate a crisis. Anaesthetic agents: need altered doses of various ones. Lignocaine okay. Epidural safer than GA

Answer 596

Posterior reversible encephalopathy syndrome Associated with PET / eclampsia Vasogenic brain oedema Occipital lobe affected most: cortical blindness, seizures, headaches Resolves on its own Seen on MRI Managed with MgSO4

Answer 597

10 fold increase in incidence in pregnancy Unilateral lower motor neuron lesion of the facial nerve (VIIth) Unilateral facial weakness including loss of frontalis muscle (can't wrinkle forehead on affected side) - Pain around ear or loss of taste on the anterior two thirds of the tongue Most cases occur around term Most due to latent HSV1 and herpes zoster which are reactivated from cranial ganglia sometimes peripartum can be becasue of swelling of the facial nerve within the petrous temporal bone Ramsay hunt: herpes zoster of the geniculate ganlgion and causes a unilateral facial palsy with herpetic vesicles in external auditory meatus - always examine ear becasue shouldn't give steroids if vesicles in ear 90% improve spontaneously Can give steriods (asap)

Answer 598

Mild to moderate: Psychological therapies: CBT, interpersonal psychotherapy - high quality evidence for mild to moderate depression Structured psychoeduation - strong evidence Low quality evidence: pscyhotherapy on mother-infant interactions, social support groups, physical activity, directive counselling, post traumatic birth counselling, complementary therapies: omega 3 fatty acids, st johns wort, acupuncture Moderate to severe - Start with pharmacological intervention and then introduce psychotherapy once medication effective - SSRis first line, TCAs second line - both low risk during pregnancy and BF - SSRIs increase extracellular level of serotonin. No increase in neonatal mortality. Not associated with major or cardiac abnormalities. no association with SGA. Paroxetine - linked to cardiac anomalies and miscarriage Possible increase in PTB Neonatal outcomes with SSRI use: possible convulsion in newborn Persistent pulmonary hypertension, resp distress, poor neonatal adaption (irritability, sleep disturbance, crying, tachypnoea, hypoglycaemia, poor thermal regulation, occasionally seizures - mild and self limiting. within 72h) Strong evidence to use SSRIs and TCAs when BF Recurrence rate 1:2 - 1:3 in future pregnancies

Answer 599

Screens for risk of depression or anxiety - Mental health history - History of physical, sexual, emotional abuse or neglect - Level of practical and emotional support from partner - Anxiety and perfectionism levels - Stressor / losses in last year (e.g. bereavement, separation etc)

Answer 600

Mild to moderate: psychological therapies including CBT, interpersonal psychotherapy and psychodynamic education. Moderate to severe anxiety: SSRIs then introduce psychological therpay TCAs can be considered if worked well for patient previously Benzos if severe panic attacks. No evidence of malformations. Should only use for a short period as addictive e.g whilst awaiting onset of SSRIs or TCAs Risk of poor neonatal adaptation syndrome increased with benzos

Answer 601

A - large number of pregnant women take, no increased malformations B1: limited number of studies, no increased malformations, animal studies: no increased risk of malformations B2: limited number of studies, no increased malformations, animal studies lacking evidence, no icnreased risk known B3: limited number of studies, no increase of malformations known, andimal studies show an increase in malformations but ?significance C: MOA predicts harmful effects without malformations. May be reversible D: Suspected to or have caused malformations or irreversible damage. Not absolutely contraindicated X: high risk permanent harm. Do not use

Answer 602

Preconception counselling: drugs and alochol cessation, educaiton about risks in pregnancy, edcuation about raising a child in context of mental illness, appropriate contraception until ready to have a baby, Multidisciplinary team input Psychoeducation and supportive therapy CBT and interpersonal psychotherapy and psychoeducation important if secondary depression or anxiety Pharmacological treatments - Antipsychotics: dopamine blockers. (Excess dopamine = psychotic symptoms) First generation (typical) antipsychotics: haloperisol, chlorpromazine - not selective and block dopamine receptors along severeal neural pathways casuing unwanted SE Second generation (atypical) antipsychotics: clozapine, risperidone, olanzapine, quetiapine, arirpriprazole. More selective dopamine antagonists and also have sertonergic properties. less side effects SE: sedation, weight gain, metabolic syndrome, diabetes, hyperprolactinaemia Extrapyramidal SE: akathisia, dystonism, parkinsonism, tremor Limited evidence for safety for all antipsychotics: no known to be associated with adverse outcomes. Some studies show increase SGA, GDM, PTB, CS. Neonatal adaptation syndrome Clozapine: don't use. Crosses placenta. Causes agranulocytosis. BF: need to monitor infants WBC count Risperidone: probable cardiac malformations. Quetiapine: incrased risk miscarraige. Anticonvulsants: NTDs, cardiac, orofacial, urinary tract, skeletal. Valproate facial abnormalities. 5mg folate / day Lithium: Antenatal monitoring of lithium recommended as requirements increase during pregnancy (narrow therapeutic range). >1.2mmol/L can cause toxicity and presents with nausea, vomiting, cramping and sometimes diarrhoea. Acute toxicity: neuromuscular signs. Cardiac dysrhtymias Ensure adequate fluid intake Monitor levels every 4 weeks, then weekly from 36 weeks Renal impairment can cause toxicity Women should give birth in hospital Epsteins anomaly (septal and posterior leaflets of TV displaced) HIGH RISK OF NEONATAL TOXCITIY WITH BREAST FEEDING. Take carbamazepine or sodium valproate. Sudden increase in lithium at birth as fluid balance shifts. Adjust dose just prior to onset of labour and aim to recommence treatment immeedaitely after the birth at the pre pregnancy dose. Don't give lithium in labour as increased placental transfer rates. Check levels 12 hours post dose, post delivery, before being reinstated

Answer 603

1:1000 Acute onset of mania with pyshcosis Starts as disordered behaviour, change in mood, insomnia, agitation, then full blown mania with dleusions, hallucinations, disorders speech etc 25% risk if BPAD 50% if previous psychosis 75% if BPAD and first degree relative who has had pp psychosis Psych emergency - all should be admitted to psych ward High risk infanticide and suicide Peak onset <7/7, up to 90 days and can last for months Ddx: cerebral or systemic disorder: eclampsia, infection Exogenous toxins Baby blues ``` Treat as soon as recognised Lithium antipsychotics anticonvulsants antidepressants 50% will develop BPAD ```

Answer 604

CHC: 99.7% perfect users, 91% typical POP: 99% perfect use. 1.41 pearl index for levonorgestrel, 0.17 for desogestrel Copper: 99 - 99.9% Mirena: 0.1 pearl index. Progestogen only implant: 0.05% Depo provera: 0.2% perfect use, 6% typical use Emergency contraception - Levonorgestrel 1.5mg - 2.2% pregnancy rate if taken within 96h. Doesn't work if already ovulated as works to delay ovulation - Ulipristal acetate 30mg (selective progesterone receptor modulator). 1.4%, works up to 120h - Copper: <1%. Works if put in 5/7 from UPSI or 5/7 from ovulation. Need to put in pre implantation.

Answer 605

1: Norethisterone 2. Levonorgestrel 3. Desogestrel, cyproterone acetate, getogene 4: drosperinone, dienogest - spironolactone analogues - mild diuretic effect Some of the later generations have higher risk for VTE because they potentiate oestrogens effect on liver anticoagulant production - 8,9,10 And have anti-mineralcorticoid effects - dehydration No evidence to choose a later progestogen as first line cyproterone fewer androgenic effects If have sex before missed POP / wihtin 24h of it don't need ECP becasue sperm only lasts in the genital tract for a few hours. If you have sex >27h after missed pill then do need ECP Only UKMEC4 = breast cancer UKMEC3: IHD, stroke, previous breast cancer, severe liver cirrhosis, HCC

Answer 606

``` 3500 people in Aotearoa with HIV Acute infection (50%) fever, rash, lymphadenopathy, pharyngitis, myalgia, arthralgia, headache ``` Asymptoma infection many years Immune deficiency: multiple symptoms related to declining CD4 counts: oral thrush, diarrhoea, weight loss, skin infections, herpes zoster Complications: AIDS: opportunistic infections such as pneumocystic jiroveci pneumonia, oesophageal candidiadsis, cerebral toxo, cancers such as kaposi sarcoma, death Test 6/52 following encounter ``` If positive - CD4 count - normal is >500 HIV virla load HIV resistance testing Standard biochem, glucose, lipid, urinarlysis, Hep A, B, C TB ``` ``` ART gives similar life expectancy free counselling and support Discuss prevention of transmission and contact tracing Discuss duty of disclosure: no leagal obligation if condoms are used, or once there is an undetectable viral load for 6 months or more. Referral to ID Notifiable infection Address mental health needs ART ```

Answer 607

To diagnose bacterial vaginosis 3/4 Clue cells on microscopy Whiff test positive: amine test with KOH - releases amines - fishy smell Offensive vaginal discahrge Vaginal pH alkalaine >4.5

Answer 608

``` Gardnerella vaginalis Mobiluncus Peptostreptococcus Fannyhessae vaginalis Mycoplasma hominis Ureaplasma Prevotella Atopbium ```

Answer 609

Nothing: 30% of patients will clear over 6 months Cryotherapy: repeated once weekly until clearance - only treatment suitable in pregnancy Podophyllotoxin 0.5% solution: twice daily 3 consecutive days, 4/7 rest, continue for max 5 weeks Immiquimod: 3 x / week alternate days, wash in morning. Can be used up to 18 weeks, although majority will clear warts by 8 weeks. monthly review recommended. local skin reactions common

Answer 610

Any sexual act, attempt to obtain a sexual act, unwanted sexual comments or advances, or acts to traffic or otherwise directed against a person's sexuality, using coercion, by any person regardless of their relationship to the victim, in any setting, including to but not limited to home and work

Answer 611

1. Reproductive health 2. Mental heatlh 3. Behavioural: e.g. hihg risk behaviour (UPSI, consensual sexual initiation, multiple partners, alcohol and drug use, obesity and inactivity, avoidance of preventative health care e.g. smears, education and employment 4. Fatal outcomes: suicide, pregnancy complications, unsafe abortions, AIDS, murder during rape, infanticide of a child born of rape 5. Physical health complaints: abdominal pain, IBD, vaginal pain, headaches, MSK etc

Answer 612

1. Belief 2. Normalisation of their response 3. Validation 4. Restoring control 5. Coordination of victim support

Answer 613

NEJM 2019 Multicentre randomised controlled unmasked trial Conducted because unclear evidence of benefits for IOL between 39 and 41/40 <39/40 - worse perinatal outcomes >41/40 increasing perinatal risk Aim: does elective IOL at 39/40 result in a lower composite outcome of perinatal death or severe neonatal complications than expectant management among low risk nulliparous women Included women 34 - 38+6 6000 women Modified bishop score calculated and women assigned 1:1 to IOL at 39-39+4 or expectant management until 40+5, delivery no later than 42+2 Primary outcome: composite of perinatal death or severe neonatal complications including - perinatal death - resp support in 72h - apgar <3 at 5 mins - HIE - Seizure - Infection - Mec aspiration - Birth trauma - ICH and subgaleal - Hypotension RR 0.8 for IOL group - NOT ss as CI crosses 1 Maternal outcomes: - CS - RR 0.84 in IOL group ss - Hypertensive disorders: RR 0.64 in IOL group ss Conclusion: no ss difference in frequency of primary outcome ss lower amount of CS and hypertensive disorders of pregnancy NNT to avoid one CS = 28 Strengths: Large trial with ability to detect differences that previous trials have not. Various bishop scores. Varieties of IOL protocols making results generalisable Limitations: blinding not feasible, not powered to detect infrequent outcomes, cost effectiveness not included

Answer 614

RR 0.33 for SB NNT 426 RR 0.92 for CS NICU admission RR 0.88 5 min apgar score RR 0.7 Mec aspiration less

Answer 615

10. 8 / 10,000 ongoing pregnancies | c. f 2.1 at 37

Answer 616

offer by 24h - RANZCOG Cochrane - Reduced infectious morbidity, neonatal sepsis, NICU admission Nil other differences

Answer 617

NEJM 1996 Multicentre RCT 5000 women Induction of labour compared with expectant management for prelabour ROM at term Intervention arms - Labour induced immediately - oxytocin - Labour induced immediately - PG x 2, then oxytocin - Expectant management for 4/7 - then oxytocin (IP or OP monitoring) - Expectant management for 4/7, then PG gel Outcomes - Primary: definite or probable neonatal infection Chorio 2 x less likely in IOL with oxy group and less likely in PG IOL group - Secondary : CS - no difference Also looked at other measures of maternal, fetal, neonatal health IOL with oxy = shortest time to delivery No difference in neonatal infection with IOL compared to expectant management

Answer 618

No dopplers avaialble 38/40 UAPI abnormal 37/40 MCA, CPR or EFW <3rd 38/40 SGA fetsu with normal dopplers and EFW >3rd, by 40/40 This is MOH guideline

Answer 619

ARM and ocy fastest method Vaginal miso best for achieving birth within 24h but higher rates of hyperstimulation Balloon least effective Oral miso least likely to require CS

Answer 620

Established labour: Primigravida should have 0.9cm / hour Multip 1.2cm / hour

Answer 621

GS ≥25mm and no YS Embryo ≥7mm and no FH FU scan Embryo present and then 7/7 later no cardiac activity GS MSD ≥12mm with no embryo and a repeat scan in 7/7 no interval development of YS or embryo YS present and then 11/7 later no embryo with FH MSD <12mm with no embryo and 14/7 later no YS or embryo absence of cardiac activity previously seen

Answer 622

50% chromosomal abnormaliteis

Answer 623

Advantage: avoidance GA, invasive surgery, feeling of control Disadvantage: unpredicatble outcome and timecourse, bleeding heavy and painful often, emergency surgery No differneces risk of infection duration can be as long as 6-8 weeks

Answer 624

Conservative 65% missed, 80% incomplete Medical 84% Surgical 97%

Answer 625

APLS ab Karyotype on POC, then reflex testing of parental chromosomes if unbalanced strutural chromsomal abnormalities are found. USS: anatomical factors Thrombophilias: e.g. F V Leiden, Prothrombin gene mutation, Protein S

Answer 626

No evidence for first trimester progesterone therapy to prevent miscarraige in an unselected population Progesterone supplemntation until second trimester in women with threatened miscarriage reduces rate of spontaneous miscarraige and may be consdiered Recurrent spontaneous miscrriage - no improveed outcome (PROMISE trial) Luteal phase support with synthetic progestgoens should be used in IVF

Answer 627

Steroid dervied from norethisterone - blocks progesterone, a hormone necessary for continuation of pregnancy Senstizes the myometrium to prostglandins, increases uterine contractility and softens and dialtes cervix

Answer 628

Synthetic prostaglandin E1 analogue

Answer 629

Smith 2010 - Blood Aspirin and Heparin for Recurrent Miscarriage RCT Inclusion: ≥2 pregnancy loss <24/40 and currently <7/40 in pregnancy excluded endocrine, anatomical, chromosomal, immunological cause for recurrent miscarraige Interventions - Aspirin and LMWH 40mg daily + intensive surveillance - Intensive surveillance Outcome: pregnancy loss 294 women No reduction in pregnancy loss with intervention

Answer 630

Aspirin + heparin or aspirin alone in women with recurrent miscarriage NEJM 2010 Background: 1% of women have ≥3 miscarriages, 5% have ≥2 miscarriages 50% no underlying cause found RCT Age 18-42, ≥2 miscarriages <20/40 Unexplained Intervention: 80mg / day of aspirin from randomization until 36/40 and LMWH from 6 weeks until labour OR Aspirin alone OR Placebo Primary outcome: live births Secondary: miscarraige, IUFD, PET / HELLP, SGA, abruption, PTB, thrombocytopenia 364 84% became pregnant 54% had live birth No difference in any of the groups combination therapy delivered on average one week prior to placebo

Answer 631

A comparison of medical management with misoprostol and surgical management for early pregnancy failure NEJM 2005 Chang et al 625 women in frist trimester with missed or incomplete miscarraige RCT 800mcg vaginal miso (+ second dose if incomplete and vacuum day 8) vs vacuum aspiration 3:1 ratio Outcomes: completion of miscarraige / treatment failure SE ``` Results: success rate miso 85% SE toelrable 78% would use miso again maternal outcomes rare - similar between grouwp ``` Miso is a safe and acceptable method of miscarraige management Strengths: RCT Limitations: Not our critreeia for medical management miscarraige

Answer 632

Fibrinogen is converted to fibrin and makes a clot In trauma, tissue plasminogen activator is released and this converts plasminogen to plasmin. Plasmin breaks down fibrinogen and fibrin TXA inhibits plasmin

Answer 633

Retrosepctive study that groups people into case (outcome) vs control (non-outcome) Prone to bias Best for a rare slowly progressing disease, because you are looking at the end

Answer 634

Prospective data collection Compares exposed vs non exposed Prone to bias