Womens Health

Combined oral contraceptive pill: COCP: < 48 hours: can take 2 pills on same day. >48 hours: 2 pils on same day + condom for 7 days

-low dose estrogen > negative feedback on FSH > low fsh > cant cause follicular development to release estrogen from granulosa cells that promote endometrial development > thus endometrium thins -Low dose progesterone > decreases LH > prevents ovulation > thins endometrium and thickens mucus. Admin: -daily administration for 21 days -7 days of sugar pill to allow the normal bleed: these r much lighter bc only very small amounts of estrogen facilitate endometrial establishment -can be started at any time during the cycle but barrier methods (condoms) should be used until the first applied until first period. -if u start it 5 days within getting ur period, you are protected from pregnancy -If u start it at any other time, u need to take pill for 7 days until you are protected. Make sure you use other barrier methods such as a condom Missed a dose dose <48 hours: can take 2 pills on the same day -if one hormonal pill is missed <24 hours from the time it should have been taken or <48 hours 1. Take late pill as soon as possible 2. Continue taking same pill at same time even if it means taking 2 pills on the same day 3. No contraception is needed Missed dose >48 hours: can take 2 pills in the same day and use condoms until pill have been taken for 7 days. 1. Take recent missed pill ASAP 2. Continue taking same pill at the usual time (even if it means taking 2 pills in same day) 3. Use barrier (condoms) or no sex until taken the pill for 7 days 4. If pills were missed on the 3rd week, omit taking sugar pills and go onto taking the hormone pills, then start a new pack. *Failure rate: if taken perfectly > 0.3% failure rate: 3 in 1,000 get pregnant after 1 year. Typical use > 9% failure rate: 9 in 100 get pregnant in 1 year. If difficulty with compliance > transdermal patch or nuva ring is ALTERNATIVE COCP Benefits: 1. Lighter, less painful periods 2. Decrease risk of ovarian and endometrial cancer 3. Decrease ectopics 4. Controls Acne bc of suppression of LH and androgens 5. Fertility returns when stopped -Levlen is most commonly prescribed pill: good at controling periods. It is a second generation out of the 4. -Yaz is another common one. 4th generation. ^'ed anti-androgenic properties to control weight gain, bloating, acne better. Use in PCOS. Risks: 1. Increase risk of DVT (blood clots): increase risk of blood clots in deep veins of legs or arm that can travel and get stuck in the lungs thus NOT suitable in women >35. 3. ^ risk of breast and Cervical cancer: C for cervical cancer/C for COCP 4. ^ risk of cholestasis, cystitis 5. Nausea, depression and mood changes, breast tenderness, headache, bloating. Most resolves within a few months (2-3 cycle) Loss of efficacy with alcohol, anticonvulsants, mood stabilizers, antibiotics *Cant be used during lactation. CONTRAINDICATIONS: Absolute NO: 1. Pregnancy or breast feeding (6 months) 2. Smoker >35 yrs: >15 cigs per day 3. Uncontrolled HTN: moderate/severe HTN 4. Hx of VTE/DVT 5. Ischemic heart disease, or stroke 6. Migraine with neuro sxms 7. Breast cancer 8. Diabetes w/ retinopathy/nephropathy/neuropathy 9. Severe cirrhosis or liver tumor Relative contraindications 1. smoker over the age of 35 (< 15 cigarettes per day) 2. Migraine with aura 3. Gall bladd disease ******Gina presents with 2 months of spotting after u put her on OCP Break through bleeding (spottin) occurs in the first three to six months!!!!!! Missed 2 days in a row: take 2 pilsl in same day and use condoms until taken 7 days in a row of the pill If missed pills on week 3, dont take sugar pill, keep taking the hormone pill then start new pack.

Diabetes in pregnancy

-T1DM, T2Dm, Gestational Diabetes *glycemic levels drop after placenta has been delivered thus DONT give insulin or else mom will hypo. Physiology: -as preg progresses, an increase in size of placenta w/ a rise in hormones at around 26 weeks of pregnancy >> estrogen (very weak impact), prog (strong), cortiosol (very strong), hPL (strong) (human placental lactogen) causes an increase in insulin resistance > causes an increase in beta cell hyperplasia -fat storage increases in mom > hPL stimulates lipolysis >> production of glycerol and free fatty acids for fetus >> diabetogenic state of pregnancy -T1DM and T2DM cant respond to the increased need for insulin production thus lead to hyperglycemia unless they get exogenous insulin. -Borderline pancreatic reserve or conditions w/ ^ed insulin resistance (obesity) > it is possible for endogenous insulin to be inadequate > thus lead to gestational diabetes. -ketoacids cross placenta during starvation in mom -Maternal glucose crosses placenta thus lead to overweight babies. -maternal hyperglycemia leads to A. Fetal hyperglycemia B. Fetal beta cell hyperplasia and hyperinsulinemia C. ^ed fetal growth and ^ed rx of 1. fetal death in utero 2. RDS: fetal hypergly and hyperinsulinemia > delays lung maturation (effect on pulmonary surfactants) 3. Hypoglycemia 4. ^ed neonatal morbidity Neonatal risks: Hyperglycemia in pregnancy > can cause congenital malformations > accounts for 30-50% of PNM (perinatal mortality -incidence of major anomalies > 5-10% -insult occurs before 7 weeks gestation (occurs before they know they are pregnant thus important to keep levels normal) Can impact: 1. CNS > anencephaly/spina bifida 2. Cardiac anomalies: MOST COMMON MALFORMATION: VSD, transposition of great vessels 3. Sacral agenesis or caudal regression syndrome: 200-400X ^ed rx in T1DM -Macrosomia: >90th centile for gestational age: 40% of IDDM preg (T1DM). Delivery of infant >4.5kg occurs 10X more than in non diabetics. -shoulder dystocia -traumatic birth injuries -rate of macrosomia ^'s as BSLs rise *control of BSLs w/in normal range reduces neonatal morbidity and mortality *GDM leads to childhood obesity -fetal death: still birth rate of 10-30% in IDDM (T1DM): due to chronic intrauterine hypoxia due to alterations in RBC oxygen release and placental blood flow. ^ed incidence of IUGR in diabetic vasculopathy -^ed incidence of pre-eclampsia -fetal asphyxia: fetal hyperinsulinemia: ^ in O2 consumption > decrease in arterial O2 content >> ^ in fetal metabolic rate and O2 requirement where there is reduced placental blood flow and fetal oxygenation. -neonatal hypoglycemia: due to rapid fall in plasma glucose after clamping of cord -neonatal hypocalcemia > lead to decrease in PTH production and reduced magnesium levels Maternal risks: 1. Nephropathy: -reduced Creatinine clearance and or proteitnuria -^ed Pre-eclampsia, IUGR and pre-term baby -ACEi is C/I > reduce intraglomerular pressure/teratogenic 2. Proliferative retinopathy: -2x rx of progression in preg if mom had prolif retinopathy prior to preg (T1/T2DM), vision deterioration > need eye review during preg. 3. Coronary artery disease: women w/ CAD r at ^ed rx of death during preg. Pathophys: -hyperglycemia > alters oxidative metabolism > increases free oxygen radicals in deveoping fetus which is teratogenic *obesity and GDM: -adipose tissues produce > adipocytokines: leptin, adiponectin, IL6 > a/w changes in insulin resistance Risk of developing GDM: -2.14X higher in overweight women -3.6X in obese women -8.6X in morbidly obese women Mx: Pre-pregnancy: -since fetal anomalies (CNS,Cardiac, musculoskeletal) occurs during first 7 weeks of pregnancy > pre-pregnancy counselling should occur aiming for HbA1C <6.5% before conception. -glycemic control -folic acid supplementation: 5mg/day due to ^ed rx of NTDs. -HbA1C levels correlates between rx of congenital malformaitaon: HbA1C >8% >> 8% ^ed rx of major malformation. >10 >> 24% rx of mal. -aim for normoglycemia w/ BSLs: A. Fasting: <5.5 B. 2hr post meal <7 -insulin injections: short and long acting insulins and CHO counting -Dietary advice -Aim for vaginal birth(induction of labour) term delivery between 37-40 weeks: give steroids for fetal lung maturity if LUSCS prior to 37 weeks -aim for glucose control prior to labor and during labor : combo of insulin and dextrose Fetal surveillance: Monash protocol: Bi BI ****ing ****: biometry, biophyiscal, fetal movements, CTG if abnormal BPP 1. Biometry (US fetal size): @ 28/32/36 weeks gesat 2. Biophysical profile: fetal movements/tone/breathing/AFI: amniotic fluid index > indicator of fetal well being: weekly from 34 weeks. -CTG if Biophysical profile BPP is abnormal 3. Umbilical artery blood flow weekly from 34 weeks 4. Fetal movements -US assessment of fetal size aid timing of delivery Macrosomia/IUGR Macrosomia > ^ rx of shoulder dystocia/CPD (cephalopelvic disproportion): rx ^'s as >4kg -selective organomegaly w/ increases in insulin sensitive tissues (fat/muscle/liver) -disproportionate ^ in abodomen circumference and shoulders. ***IUGR : more common in IDDM (T1DM) w/ microvascular disease due to ^ placental resistance >>resulting in growth deficiency T1DM: ^ed rx of IUGR and macrosomia D: ^ed rx of macrosomia Gestational Diabetes: -90% of cases of diabetes in preg -rx of develop glucose intolerenace later in life -50% develop T2Dm in 15 yrs -GDM: defined as restricted to preg and dx during preg Dx of GDM: Performed at 26-30 weeks: OGTT: Fasting> 5.0 mmol/l 1 hr >9.9 2 hr >8.4 *in women w/ Phx of GD do OGTT at 10-14 weeks and repeated at 28 weeks : if negative still does second one Pathophys: -inusulin resistance as w/ T1DM due to ^ production of cortisol, hPL, progesterone + due to obesity mx: -diabetes educator -monitor BSLs in morning then 2 hours after meals. Aim for normal BSLs: *Aim btwn 4-7 and fasting <5.5 -dietary advice -exercise -if well controlled GDM > low rx of fetal cxs -GDM requiring insulin: ^ed rx similar to uncomplicated IDDM preg -fetal surveillance: require insulin, other cxs, weekly Biophysical profile: fetal movemtns/tone, biometry @ 28/32/36w. CTG if abnormal BPP. Timing: A. GDM on diet alone > await onset spontaneous labour B. GDM requiring insulin: depend upon fetal growth and glycemic control:

Menopause:

-cessation of menses for 12 consec months w/o other reason for amenorrhea (pregnancy, HRT or other medical condition) -permanent cessation of ovarian fxn in bilateral oophorectomy> surgical menopause or medically by chemo/radiotherapy (tx induced menopause) -Perimenopause: years before and after cessation of menses in an ovulating women marked by irregular menses and menopausal sxms. Epi: avg age is 51 Hot flushes most common sxm Aetiology: women r born w/ set of oocytes > when depleted during early 40's > ovarian production of progesterone, estrogen, testosterone declines. Fertility declines too. -Before menopause, estradiol is predominant estrogen and levels r at 100 picograms/ml -After menopause, estrone, derived from estradiol metabolism in liver and in adipose tissue become dominant estrogen and levels r 30-50 picograms/ml. Sxs: hot flushes, urogenital atrophy due to decreasing estradiol Pathophysiology: -decline in estrogen r a/w sxmomatic urogenital atrophy, epithelial thinning, decreased secretions and reduction in vaginal elasticity and increase in pH >6. -Get dryness, itch, d/c, painful sex. Thinning of vaginal epithelial can lead to tear in intercourse. -Bone resorption accelerates > > rapid decline in bone density in 3-5 years after the final menstrual period. -corticosteriod use increases rx of fractures. -mortality from cardiovascular disease increases w/ onset of menopause driven by change in lipid profile w/ an increase in LDL and decrease in HDL. #Menopause: natural event occuring between 40-60, avg 51 yrs > represents permanent cessation of menstruation and ovulation #Premature menopause: before age of 40, occurs spontaneously or due to surgery (bilateral oophorectomy), radiation of pelvis, chemo, autoimmune disease, fragile X syndrome, idiopathic. Give COCP until age of 50. #Premature ovarian insufficiency: amenorrhea, hypo-estrogenic, high gonadotrophins (FSH/LH) due to decline of ovarian fxn before age of 40. #Perimenopuase: menstrual irregularity and periods of amenorrhea due to declining progesterone and estrogen levels, and ends 12 months after the final menstrual period. (FSH and LH levels will be high but low estrogen and progesterone levels bc no more eggs) -birth: 1 million follicles -puberty: 400,000 Anti-Mullerian hormone: AMH: released by antral follicles to suppress suroudning ones. More follicles > more AMH secreted. -use this as a function of ovarian reserve. -In menopause > number of follicles r low/absent > thus AMH will be low. =Low AMH can be seen in irregulatrity and elevated gonadotropins -Low progesterone due to decreaesd number of follicles > thus get increase in GnRH (FSH) trying to increase follciles. -Decrease in estrogens, Low estradiol (E2) and predominance of Esterone (E1) in adipose tissue and liver. -low estradiol and progesterone > High GNRH > high FSH and LH ***From perimenopause to menopause: get rise in FSH and LH, decline in in Estradiol E2, and testosterone and estrone E1 remain stable. After menopause: FSH and LH rises then plateus, E2 declines, E1 and Test stays stable. *Estradiol maintains tonic inhibition of thermoregulatory center in hypothalamus. Decline in estradiol > lose inhibition > lowers threshold for feelings of temp, sweating, peripheral vasodilation. -Hot flashes last 7 to 11 years -Estrogen is lipo-protective: decreases LDH and increases HDL cholesteroel. -Also get bone loss RFs: -age 40-60 -chemotherapy/radiation: cancer tx -smoking -ovarian surgery: oophorectomy > menopause -FHx Hx: -Rfs -amenorrhea: >12 months -irregular menstrual cycle during late 40's marks entry into perimenopause: heavier/lighter periods, intermenstrual bleeding -hot flushes and night sweats: vasomotor sxms (hot flushes/night sweats) may begin several years before menopause and many years after menopause -dryness, itching, dyspareunia due to low estrogen -mood changes: irritability -sleep disturbance Ixs: Clinical dx: amenorrhea >12 months -pregnancy tect: urine hCG -FSH: in women <40 yrs -serum estradiol: predominent estrogen before menopuase. Mx: saves weight, COCP/transdermal estrogen, ovestin topical estrogen (no need to use progesterone for topical) 1. Lifestyle: Saves Weight: loes weight, exercise more: both benefit CVS and overal wellbeing. -avoid spicy foods, caffeien, stress. OH and caffiene can worsen hot flushes -layered clothing, fans, cold water, is helpful. Exercise to prevent osteoporosis, calcium and vitamin D 2. COCP: any women with intact uterus must receieve est and progesterone to prevent endometrial hyperplasia (low prog and high estrogen)estrogen will reduce hot flushes by 90%. In pts who have had amenorrhea >12 months. If pt had breakthrough bleeding >6 months > do endometrial assessment (pelvic US +/- endometrial biopsy) 3. Topical estrogen for vagianl dryness/itch: ovestin cream -OR Transdermal estrogen in pts who have risk of thromboembolism (BMI>30), risk of gallstones or adheering to pills. -SEs: headache, infection, breast pain, N, insomnia. -2nd line SSRI in women who cant take hormone therapy > Escitalopram or paroxetine reduces hot flushes -3rd line: Gabapentin -4th line: clonidine: antihypertensive, alpha 2 agonist > decrease peripheral resistance HR and BP and reduces hot flushes ****CLonidine: Catecholamine Lowering. Anti-SLUD from alpha 2 agonism: anti-salivation, lacrimation, urination, defecation. ***COCP: protects against ovarian and endometrial cancer -Increases risk for breast and cervical cancer. ** Perimenopausal => CYCLICAL HRT: meaningg we give estrogen for first 14 days, then progesterone until day 28 to mimic normal cycle. **Post menopausal women => Continuous HRT w/o no withdrawal bleeds bc of decreasing risk of malignancy. Progesterone can be oral, implanon or mirena. *Have Uterus > COCP or transdermal estrogen -No uterus: estrogen alone. **Women is considered potentially fertile for 2 years after her last menstrual period if she is under 50 years and for 1 year if she is >50. -<50 + no risk of DVT > COCP: relief from menoapausal sxms and protection of contraception ->50 shouldnt be given COCP Stopping therapy: -review every 2 yrs -risks of breast cacner and thromboemobilism rise and r equal benefits at 5 yrs -switch from COCP to progesterone only after age of 50. -Tibolone: can replace HRT but vascular risk is > than HRT.

Dysmenorrhea (painful period with cramps) DDX

1. Primary dysmenorrhea: occurs at the onset of menstruation in absence of any Pelvic disease. *Cramping pain, bloating, N/V,headache 2. Secondary dysmenorrhea: adeno, endo, leio, pio, ecto -Endometriosis: most COMMON cause of painful periods. Tissue outside of uterus. *cyclical pain, dyspareunia (pain w/ sex), constipation, infertility - Leiomyoma (fibroids): Benign smooth muscle tumors inside uterus: *heavy periods, fullness in pelvis, urinary freq -Adenomyosis: enlarged uterus on palpation. *Heavy, spotting, pain w/ sex? -PID: PHx of STI, pain during sex? Discharge, spotting, F/N/R -Ectopic: sudden peritonism? Light headed, dizzy, pale, cold

Female infertility Ix's

1. Urinary Beta-HCG

Emergency contraception

1. Progesteron only (postinor): (Plan B) -oral high dose 1.5mg levonoregsterel (progesterone from mirena but high dose). -2 tablets > take both -taken w/in 3 days of unprotected sexual intercourse. Sooner the better -morning after pill suppresses ovulation and thickens mucus but the key is that it is only supressing ovulatiotn, not preventing fertilization. -Sperm lasts 72 hours in genital tract and longer u wait post intercourse > the longer u give fertilizaitaon to occur. -If u vomit <2 hours after taking it, repeat the dose. Take antiemetics 1 hour before emergency contraception. Benefit: 1. Available over the counter with no age limit 2. 3 days to take first dose and efficacy remains for 5 days. 3. No CI cons: 1. Slight risk of ectopics 2. Vaginal spoting, N, abdo cramps 3. May change in timing of menstrual cycle. Next period slightly late 4. If you have ovulated already, it wont prevent fertilization and implantation from occuring! 2. Yuzpe: Combination Levonorgesterol and Estrogen: -Inhibits ovulation > need to be taken within 3 days of sex -less effective and less common than plan B. -2 tablets taken 12 hours apart. Cons: -makes u very nauseous. -less effective -2 doses 12 hours apart. 3. Copper IUD: -prevents fertilization from occuring as well as disrupts endometrium to stop implantation -admin upto 5 days post sex -dont at clinic Beenfit: 1. Increase window of efficacy 2. Provide longer acting contraception for 10 years Cons: 1. Heavier more painful periods 2. risk of infection. ****Termination of pregnancy services or routine care is available if these methods fail -normal period may be 1-2 weeks late on these therapies but need to get pregancy test outside of this window. Always counsel: 1. Contraception 2. STI prevention (condoms) or sex with one partner 3. Cervical screening test 5 yearly: age 25-74: look for HPV DNA. If positive do cytology. Then send for colposcopy (look at abnormal cells under microscope after staining with acetic acid)

Conception: 8-12 weeks

Always start with: 1. Normal Medical history: PDAFO: PMHx, Drugs, Allergies, FHx, Obstetrics 2. Disease prevention: folate, vaccination, listeria 3. Screening current health: Head to toe Pre-natal: was it planned or unplanned? ->35: ^ rx of GD, Pre-eclampsia, chornic HTN, cesearan section, chromosomal abnormalities PMHx: -Heart, lung or kidney disease? BP/Diabetes -infections: TB, Rubella, HIV, hep B/C Drugs: -antihypertensives, anti-epileptics, contraceptives, FHx: GD, pre-eclampsia, ectopic, genetic abnormalities, depression Obstetric: -GPA -Pre-natal: planned or unplanned? This will give u a feeling of mothers mental state -Antenatal: length of gestation -Peri-natal: cesarean/vaginal/forceps -Post-natal: cxs: before, during, after, post natal depression, fetal abnormalities Gynecological Hx: -LNMP -Length of period 3-7 days -period regularity: 21-35 day cycle? <21 or >35 is irregular -IMB: bleeding btween periods -Dyspariunia? -Menopause: spotting, clots, flooding -Infection: Storage FUND: freq, urgency, nocturia, dysuria: burning. Obstructive SHED: stream, hesitancy, empty incomplete, dribbling Disease prevention: -folate: 3m before, 3m after -Listeria avoidance: avoid unpasturized dairy and raw meats/seafood Antenatal screening: -ask about mother wanting to keep baby if it has downs syndrome. If she does, then nuchal translucency scan is not warranted. Assess Head to to exam for major antenatal cxs: -head: Pre-eclmapsia (occurs after 20weeks)> headache, visual disturbance, light headed or dizzy. -neck: thyroid: hot or cold intolerance -heart and lungs: chest pain or sob -abodmen: N/V: should stop by 16 weeks -Urinary: UTI: burning, pain. GDM: urinary freq, thirsty -Bowel: constipaiton: common effect of preg -vaginal miscarriage/ectopic > pain in tummy? *fundal height taken from pubic symphasis and height should be w/in 2cm of weeks gestation after 20 weeks. -20 weeks: pubic symphisis to umilicus

Ectopic vs miscarriage:

Ectopic: -peritonism -high pain severity -less PV bleeding -acute onset -palpable adnexal mass Miscarriage: -cramping lower abdo or back pain -less pain -more PV bleeding -passage of POC (Clots)

Estrogen vs progesterone side effects

Estrogen: -depression/anxiety -breakthrough bleeding -fainting -HTN, -N/V -rash Progesterone: -dizziness -viral infection -diarrhea -joint pain -mood swings -acne -increased hair growth Both: -abdo cramping -breast enlargement/tenderness -swellin/weight gain. Postmenopausal women: COCP: -est and prog increases DVT, PE, Stroke, MI, dementia, ovarian and breast cancer -Estrogen only increases risk of ovarian cancer Dont use IUD in immunosuppressed or pts at high risk of infection/sepsis Oral contraceptives take about 3 months to adjust to and implants or long acting ones take about 6 months Barrier methods r the only protection against STI's: thus should be used in people without a stable partner.

Endometrial cancer (uterine cancer): most common cancer. (Endometrium > Ovarian> Cervical cancer)

Epithelial malignancy of the uterine corpus mucosa, usually an adenocarcinoma. -Non dysplastic: endometrial hyperplasia -Dysplastic: endometrial polyps and endometrial intraepithelial neoplasia -Malignant: endometrial adenocarcinoma and sarcoma Epi: MOST COMMON GYNE TUMOR in the developed world. 6th most common cancer in women -10x higher in western world bc strong a/w obesity Aetiology: endometrial hyperplasia is due to chronic estrogen stimulation unopposed by counterbalancing effects of progesterone. -Unopposed estrogen > chronic anovulation from PCOS -fat women RFs: AN OLD ****: occurs in older ladies Age: older >50: post menopausal Next of kin: FHX Obesity: BMI >30 3x the risk Late menopause, early menarche Diabetes Cancer: Lynch syndrome: hereditary non polyposis coli > mutation in MSH2 > colorectal cancer and predispose to enodmetrial cancer Unoposed estrogen: HRT or PCOS Nulliparous Tamoxifen: estrogen inhibitor: has pro-estrogenic effects on endometrium, particularly sarcoma's. Hx: 1. Post menopausal vaginal bleeding 2. Abnormal menstration or vaginal bleeding in pre-meno women 3. Abdo/pelvic pain and weight loss Cluster questions: RFs AN OLD ****: FHx of cancers, obesity, late menopause, diabetes. -Post menopausal -vaginal bleeding Pathophys: 1. Endometrial hyperplasia: just an increase in number of cells. Fat people have an ^ in estrogen production in peripheral tissue. 2. Endometrial intraepithelial Neoplasia EIN > dysplasia > malignancy. High rx of malig: 25% after 3 years 3. Endometrial polyps: similar to EIN a/w focal sensitivity to estrogen but less worrisome than EIN. Endometrial hyperplasia and dysplasia can lead to metorrhagia (bleeding between periods), menorrhagia (heavy bleeding), or menometorrhagia (prolonged excessive bleeding occuring at irregular intervals) due to disruption of endometrium during follicular phase PLUS damage to tiny BV's in abnormally enlarge tissue. Endometrial adenocarcinoma: Type 1 and Type 2: -Type 1: most common, 90%: aris from hyperestrogenism (obesity, PCOS, infertility, late menopause) > endometroid adenocarcinoma. Better prognosis. -Type 2: rare. Arise w/ endometrial atrophy mainly seen in post menopausal women. Subtypes: clear cell or serous adenocarcinoma. Poor prognosis. Endometrial stromal sarcoma: rare. Ix: 1. FBE: anemia due to ongoing bleeding, Serum CA-125 2. Pap smear 3. Hysteroscopy, dilation and curretage and histolopathology 4. Endometrial biopsy 5. Pelvic transvaginal ultrasound -menstrual: upto 3.5mm -Follicular: upto 7mm Luteal: upto 14mm endometrial thickness. Post menopausal women: A. Should be <3.5 mm B. Get concrned when >6 mm. Management: 1. TNM staging: Tumor we need a biopsy. Node and metastesis: MRI or PET scan 2. Hysterectomy and bilateral salpingo-oophorectomy: removal of uterus, tubes and ovaries before metastatic spread. 3. Lymph node sampling 4. Follow up and radiotherapy

Epithelial tumors (most important)

Epithelial ovarian cancer: cells of mullerian origin RFs: 1. BRCA 1 mutation: 40% lifetime rx of ovarian cancer 2. BRCA 2 mutation and lynch syndrome: 20% risk of ovarian cancer 3. FHX of ovarian and breast cancer 4. Never used OCP 5. Lynch syndrome Hx: 1. Rfs 2. Pelvic mass: palpable adnexal mass 3. GI sxms: urinary urgency/frequency, abdo fullness/bloating 4. Sxm >3 months 5. Ascites and abdo distension 6. Fatigue, LOA, weighht loss, Night sweats, bone pain, headache, SOB -Epi: 5% of cancer deaths among women in US and is most lethal gyne cancer. Risk for developing ovarian cancer is 2%. Aetiology: 1. BRCA 1 and 2 (Breast and ovarian cancer gene) mutation 2. HNPC: hered non polyposis coli > MSH 2 is a/w ovarian cancer Pathophys: epithelial ovarian cacner doesnt invade into organ space parenchyma but attaches to surface of organs. Implants along lining of peritoneal cavity. -Protective factors: 1. COCP and HRT: suppresses ovulation and decreases disruption of ovarian epithelium. 2. Multiparity and breast feeding 3. Bilateral salpingo-oophorectomy:: reduces risk by upto 90% bc it doesnt remove mulerrian epithelium on peritoneal surface. There is no screening program for ovarian cancer but the use of ULTRASOUND and CA 125 can be used. -Breast and endometrial tissue is sensitive to estrogen. When dysplasitc > estrogen triggers them to increase more. -Ovaries: are NOT influenced by estrogen but by FSH/LH. THUS COCP suppresses cellular activity thus protective against cancer. -Hereditary dysfunction of ovary > will also have hereditary renal dysfunction bc they arise from same cells. -on EXAM: comparative structure to uterine tubes in men is the appendage (consists of the paramesonephric duct/mullerian duct) of the testis. Stages of malignant disease: Stage 1: only epithelium of ovary Stage 2: involves ovary, tube and surrounding mesentary Stage 3: local invasion > bowel Stage 4: spread to others > liver, lungs, bones (spine) Prognosis: Poor prognosis: 5 year survival for stage 1 > 80% Stage 3: 40% Ix: 1. FBE, UEC, LFT, Tumor markers CEA 2. Pelvic ultrasound +/- CT 3. Ca 125: >35 units/ml. Not a diagnostic bc can be elevated in endometriosis, fibroids, pregnancy and ovarian cysts, pancreatic, breast, lung, gastric and colon cancers). 4. PET scan Mx: 1. Bilateral Salpingo-oophorectomy 2. Adjuvant Chemo (carboplatin and paclitaxel > for ovarian cancer 3. Follow up 4. Serum Ca125 > increasing levels may represent relapse

Pelvic Organ Prolapse (POP)

Pelvic organs of female drop down into the vagina: A. Ant compartment POP: Cervix and uterus: uterocervical prolapse: second most common: failure of uterosacral and cardial ligaments B. Post comp POP: Rectum: rectocele: 3rd most common: Dovetail sign: ant. Perineal folds r absent > damaged external sphincter. C. Bladder: cystocele: fts of urinary retentio nand obstruction of urine outflow D. Pouch of douglass > enterocele: 3rd most common E. Vaginal Vault POP: vagina prolapse > happens when u had previous hysterectomy Epi: 41% of women 50-79: 13% recurrence risk in 6 years -cystocele: 34%: most common is: anterior compartment: prolapse of post portion of bladder (cystocele) into vaginal cavity -Rectocele: 20% -Uterine prolapse: 14% RFs: -age: post menopausal women due to low estrogen and low vascularity -vaginal deliveries: Forceps > doubles risk. Higher in parous women. Every additional delivery upto 5 births increases the risk of worsening prolapse by 10-20% > childbirth causes damage to pudendal nerves, fascia that supports pelvic organs. -obesity exacerbates prolapse due to increased intra-abdominal pressure. -Previous surgery for prolapse -FHx of prolapse Hx; -Do u have heaviness, pressure feeling in vagina or lower abdo or back? -Do u have difficulty evacuating bowel or need use of digit? -Difficulty passing urine or feel u cant empty bladder fully? -Fecal incontinence? Pelvic organ prolapse staging: Stage 0: no prolapse: normal cervix sit approx at level of ischial spines. Stage 1: 1 cm above hymen Stage 2: at the level of hymen Stage 3: extends passed hymen but no further than 2cm > easily replaced Stage 4: complete eversion > more than +2cm: maximum decent > difficult to replace Ix: - urinalysis -post void residual (PVR) volume: suspected cystocele to look for comp of urethra or obstruction of voiding -urodynamics -ultrasound: assess muscle defects Mx: -Observation in milder prolapse -LStyle: weight reduction, avoid straing (constipation [ ^ water & fiber], lifting, cough), correct position for voiding/defection -pelvic floor rehab -pessary: restores prolapsed organs > first line. Should be on estrogen cream if on pessary -local estrogen w/ hypoextrogenic sxms or urethral prolapse -Review of management -Refer to specialist: surgery: vaginal: sacrospinal ligament colpopexy/hysteropexy, colpocleisis, perinorraphy, laparoscopic -follow up: recurrence rate of >30%

Post menopausal bleeding DDX and Ix

Systemic -HRT: given in cyclical dosing: estrogen alone for first 14 days then estrogen and progesterone until day 28. May get irregular spotting a/w endometrial activity. Normal for first 6 months then warrants Ix *Current HRT: is it dosed cyclically? Ovary -ovarian cancer: CA125 tumor marker or BRCA +. R they BRCA positive? Mass in bimanual exam. Uterine: -endometrial dysplasia or hyperplasia: new friable BV's easily rupture. * High BMI, FHx of breast or bowel cancer ? Cervical: -cervical ectropion: glandular cells/columnar epitheliam from inside cervical canal r present on outside of cervix. Hard to distinguish from early cervical cancer thus need to be evaluated. *post coital bleeding? Irregular spotting? -cervical dysplasia: friable tissue in transitional zone to bleed. *post coital bleed/irregular spotting. Vaginal -Atrophy and ulceration: vaginal dryness/dyspareunia? Dry vagina > topical estrogen. Ix: 1. FBE; 2. Pelvic ultrasound -premenopausal women: A. Menstraual phase: 1-4: 2-4 mm: >2mm B. Follicular phase: 4-14 : 4-7 mm: >4 mm C. Luteal phase: 14-28: 7-14 mm. > 7 mm 3. Hysteroscopy: slim instrument with a camera is inserted into cervix > able to detect abnormal tissue (hyperplastic/dysplastic lesions, take sample of tissue and even remove polyps or lyiomyomas (fibroid) -dilitation and curretage: remove POC: products of conception, cervical/uterine polyps > sent for histology to look for signs of CIN or malignancy

Pelvic Mass DDX and IX

Uterine -lieomyoma (fibroid): pressure sxms: deep pelvic pressure, urinary/bowel pressure, heavy periods -Endometrial cancer: mainly post menopausal bleeding -hematocolpos: adolescent, no menarche bleed, cyclical pain -pregnancy: sexually active breast tenderness, N/V, amenorrhea. Tubal: -ectopic RED FLAG: peritonitis, light headed, dizzy -tuboovarian absecess: F/R/N, d/c or smell, dysuria, cervical excitability tenderness Ovarian: -follicular or luteal cyst: persistent pain -chocolate cyst (endometriosis): dysmenorrhea, dyspareunia, dyschezia (constipaitaon) -Ovarian cancer (RED FLAG): persistent pain, abdo bloating, LOA, urinary freq, hirsutism, weight loss Ix: 1. First pass urine for infections 2. Urinary and serum B HCG test > exclude ectopic 3. FBE, Tumor marker CA125) 4. Pelvic ultrasound, MRI/CT: Ovarian cancers need needle aspiration and biopsy Risk calculator to asses risk of ovarian cancer -Risk of malignancy index (RMI): depend on: Menopausal status: post menopausal Ultrasound finding of >2 suggestive of malignancy Serum CA 125 cancer antigen Scores >250 = high risk of ovarian cancer

Abnormal uterine bleeding > USA IPALM CHAT PM

Uterus: 1. Infection: -PID is infection that moves up uterine cavity and ovarian tubes > mediate endometritis end salpingitis > inflam mediate bleeding between cycles *Ever had STI screen? HX of STI? Burning, stinging, pelvic pain? Discharge? F/R/N? 2. Polyp (uterine/endometrial polyp): dysplastic changes in wall of uterus a/w fragile blood supply Sxms: A. Irregular menstrual periods B. Heavy flow during period C. Bleeding/spotting between periods or after menopause D. Infertility E. Prolonged/excessive menstrual bleeding F. Bleeding after sex *Bleeding after sex? Painless bleeding? 3. Adenomyosis: cells grow inside uterus. Endometriosis: cells grow outside uterus and can cause adhesions -endometriosis like changes that invade myometrium > additional bleeding during menses Sxms: A. *Heavy/proloned bleeding, pain during sex, blood clots that pass during period. 4. Leiomyoma AKA fibroids. Benign smooth muscle tumors of myometrium. * Heavy menstrual bleeding, Menstrual periods lasting >7 days, Pelvic pressure or pain. Frequent urination. Difficulty emptying the bladder. Constipation. Backache or leg pains. 5. Malignancy: endometrial or cervical malignancies may increase amount of blood lost during menses. -pain after sex? Spotting? Fatigue? Weight loss? ******ESTROGEN THICKENS ENDOMETRIUM. PROGESTERONE Makes it vascular and glandular Anovulatory; PM 1. PCOS: High LH, Low FSH thus high estrogen thus heavier periods. *Infertility, hair growth, acne/oily skin? 2. Menopause or menarche: when did u get period? Hot flushes? Vagina dryness Systemic: CHAT: Contraceptives, hemotological, anticoagulants, thyroid 1. Contraceptives/anticoagulants *med hx and contraceptives? -implanon and copper IUD causes heavier periods, Mirena causes spotting for first 2-3 months. -anticoagulants: increased bleeding time increases rx of heavy men bleeding 2. Hematological -Von Willerbrands disease is most common bleeding condition. VWF delivers factor 8 extrinsic factor) and forms initial bonds bewteen platelets in the primary clot. *heavy periods since menarche? Gum bleeding, epitaxis? Easy bruising 3. Thyroid: hypothyroid is a/w menorrhhagea (heavy bleeding) *cold/heat intolerance

Gestational DM

-develops during preg and dx at 24-28 weeks of gestation on basis of OGTT Epi: Prev: 3.5% of all pregnancies Aetiology: during preg, due to progest, hPL, cortisol > insulin resitance increases. In most preg, pancreatic beta cells r able to compensate for increased insulin demands and normoglycemia is maintained. But in womeh who develop GDM have deficits in beta cell response leading to insufficient insulin secretion to compensiate for increased insulin demands RFs -advanced maternal age >40 -^ BMI (obesity) (rx 3x when BMI >30kg/m2): ^ed insulin resistance -PCOS -Fhx of DM -low fibre, high GI diet (sodas, carbs) -weight gain as youn adult -PHx GDM -physical inactivity -asians, black carribeans or middle easterns > high prevalence of diabetes Pathophys: -products of placenta: tumor necrosis factora alpha TNF alpha and HPL (human placental lactogen AKA human chorionic somatomammotropin) > induces maternal insulin resistance > marked in the third trimester (this is why screening is done at 24-28 weeks) -women who develop GDM have deficits in beta pancreatic fxn thus cant adapt to pregnancy. -hyperglycemia in late preg is a/w macrosomia and neonatal hypoglycemia, hyperbilirubinemia, hypocalcemia after birth and for the mother: gestational HTN, Pre-eclampsia, cesarean delivery. Ix: OGTT: Fasting >5 1 hr >9.9 2 hr >8.4 -blood pressure: GDM is a/w HTN and pre-eclampsia -urine dipstick and urinalysis: proteinuriia and glycosuria -UEC: kidney fxn > diabetic nephropathy: -ophthalmoscopy/fundoscopy > proliferative retinopathy Hx: -rfs -^ BMI -fetal macrosomia -polyuria -polydipsia Mx: -dietician -Low GI foods: wohle grains, legumes. -folate ^ to 4mg/day -exercise -ongoing contact w/ endocrinologist in T1DM for ongoing insulin. -self monitoring BSLs: aim for Fasting: <5.5 2 hr Post prandial: <7 -uncontrolled w/ diet > insulin therapy: insulin isophane and insulin lispro -Aim for normal vaginal delivery (induction of labour) -32 to 34 weeks gestation: antepartum fetal monitorinng: bi bi ****ing ****: A. Biometry (fetal size) B. Biophysical profile: fetal movement/tone: if abnormal > do CTG C. Fetal movements -Intrapartum glycemic control: before and during labour. NOrmally obstetrician/Dr will see mother: 1. After conception: 12 weeks 2. After 20 week morphology scan 3. After 26 week OGTT results 4. After 36 weeks for GBS swab -twice weekly CTG from 36 weeks In diabetics get extra: BiBi ****ing ****s: -biometry: size @ 28, 32w,36w -biophysical profile: weekly from 34w: fetal movement/tone: if abnormal > CTG - Umbilical artery blood flow: weekly from 34 weeks

Ectopic pregnancy: anyone with abdo pain > do preg test to rule out miscarriage or ectopic.

-fertilised ovum implanting and maturing outside of the uterine endometrial cavity > erodes structures and causes massive bleeding: -commonest cause of 1st trimester maternal deaths *BHCG rises more slowly when it is extrauterine. Intrauterine preg's double every 48 hours in first few weeks of preg Common site: 1. Fallopian tube 97%: 73% at the ampula, 12.5% at isthmus, 11.6% at fibria. 2. ovary 3.2% 3 abdominal cavity 1.3% -if undiagnosed or tx, lead to maternal death due to rupture of implantation site and intraperitoneal hemorrhage. *large internal ileac artery > uterine and vaginal arteries. Uterine arteries move along lateral edges of uterus to supply ovarian tube and ovary. W/ hormonal changes in preg > there is ^ed vascularity to an already well vascularized area. Rupture of these vessels can thus result in signifi consequence Epi: 1.62% in Australia -11 per 1,000 pregnancies or 1 in 100 -maternal mortality .2 per 1,000 Aetiology: 1. Pelvic Inflammatory disease (chlamydia and gonorrhea) > distorts fallopian tube anatomy 2. ^ rx of ectopic > smoking, many sex partners, IUD, tube surgery, infertility and IVF, age <18 having sex, and age >35. Pathophys: 1. oocyte migration difficulty a/w abnormal tube anatomy due to chronic salpingitis, tubal surgery (reconstruction, sterilization) 2. as ectopic grows > outer layer of fall. tube stretches > leads to tubal rupture and bleeding. RFs: ECTOPICS: PHx of ectopic preg, Chalmydia/glnorrhea infection, tubal sterilisation/tied, old age >35, PID/^ partners, infertility/IVF/IUD, cigarrete smoking, salpingitis, surgery. -PHx of ectopic pregnancy -Phx of tubal sterilisation surgery (tubes tied): due to tuboperitoneal fistula formation leadign to spermatozoa escape and oocyte fertilisation. -Intrauterine device -Previous chhlamydia or gonorrhea infections (PID) -chronic salpingitis -infertility -multiple sex partners: increases risk of PID -smoking: due to decreased immunity leading to higher rx of pelvic infection and impaired tubal motility -IVF -sex <18 yrs -advanced maternal aging: >35 years -tubal reconstruction surgery Cluster questions: -amenorrhea/breast tenderness/N/V, peritonitic pain, vaginal bleeding Hx: -sudden or gradual abdo pain: typically unilateral lower abdo pain but can be generalised or upper abdo. Pain w/ vomiting > rupture. -amenorrhea: LMP 6-8 weeks ago -vaginal bleeding -Peritonism: abdo tenderness (also present in early preg loss): gaurding > sign of rupture -adnexal tenderness or mass -hemodynamic instability and orthostatic hypotension: hypotension and tachy > sign of rupture*** -cervical motion tenderness: sign of rupture > irritation from itraperitoneal bleeding -urge to defecate: stimulation of rectum from blood pooling in posterior pouch of douglas. -referred shoulder pain: bleeding from tubes may irritate diaphragm > referred shoulder pain. Ix: -urine/serum bHCG: positive: slow rise in BHC. -group and hold + cross match: if pt ruptures ectopic > surgery ASAP -transvaginal ultrasound > location of pregnancy: can see empty gestational sac after 6-7 weeks and B HCG >1,500 is very suggestive. Mx: -DRS ABC + Resuscitation if ectopic ruptured w/ life threatening bleeding -If pt is not bleeding HEAVILY and B HCG is falling Low risk: -Expectant Mx: hemodynamically stable, asymptomatic pts (minimal pain) w/ resolution (demonstrated by platue or decrease in HCG). Resolve if HCG levels are decreasing from HCG level of <1500 IU/L Moderate or failed expectant mx or ruptured ectopic preg: 1. methotrexate: inhibits folate and prevents DNA/RNA synthesis: need to check BHCG levels to see if its dropping 2. Laparoscopic surgery or laparotomy (if severe hemodynamic instability where immediate access is required). or methotrexate in pt who is clinically stable with non-ruptured ectopic preg. > salpingostomy/salpingectomy -need to take HCG levels after salpingostomy until levels r undetectable. Neg preg test should be confirmed after salpingectomy. -if HCG doesnt return to undetectabel level after surgery > methotrexate is given Ruptured ectopic or failed medicalc mx: -hemodynamically unstable: fluid resus, laparoscopy

What defines onset of labour?

- the onset of rhythmic regular painful contracts taht increase in amplitutde and cause dilation and effacement of the cervix -a show of blood and mucus which indicates that the cervical canal is opening labour contractions: -contraction freq in active labour is commonly 3-5 in 10 minutes lasting for 40-60 seconds > anyting greater than this (tachystystole) or lasting longer (hypertonus) > risks decreased variability. Pain: -tight pelvis or back pain > this is pain from uterus -stinging burning pain > pain from perineum

Molly is 48 w/ menopausal sxms and 6 months of amenorrhea and on OCP. Should she continue it?

-Avg age of menopause is 50. -Women is postmenopausal when she has had 12 months of amenorrhea. Managing contraception in menopausal women (meopausal symptoms): Women <50: continue the contraception for 2 yearrs after last period Women >50: continue contraception for 1 year after last period.

Pre-eclampsia

-BP drops in frist trimester and second trimester at around 12 weeks and at 24 weeks: this is due to ^ in progesterone > relaxes smooth myometrial and peripheral smooth muscle > vasodilation and drop in BP. -during 3rd triemster: BP begins to rise. *Dont start BP tx until BP is severe >160/110 -syncytiotrophoblast gives rise to placenta > improper migration into endometrial wall to widen the spiral arteries do not occur thus the spiral arteries remain narrow > placental insuffiency > IUGR. -S steroids: for fetal lung maturation when <34 weeks. -T Transfer to tertiary center and admit -A Antibiotics: Benpen for GBS positive ladies intrapartum (2 dose 4 hrs apart) -T Tocolysis: not in this context -I: Intrapartum care for mom and baby -N- Neuroprotection Magnesium Sulphate useful for baby when <30 weeks. Given to women who have to deliver preterm <30 weeks Convulsions during delivery: -if u can control seizures w/ MgSO4 then there is no CI to vaginal delivery. If poor control. >may need to do cesarean. Post natal Mx: 1/3 of all eclamptic seizures occur AFTEr delivery (in that 6 week post partum)) period -continue tx for 6 weeks or until resolved -eclamptic seizrues occur 24 hrs post partum -weekly follow up for 6 weeks: with PE screen: BP, urine dipstick -education and rx of recurrence: 50% recurrence rate but may be less severe. Make sure treating them early in pregnancy >take aspirin.

Androgen insensitivity (XY)

-Baby XY produce testis but has testosterone insensitivity thus cant change vagina to penis. Thus baby has vagina. -The AMH prevents uterus formation. -Excess testosterone from the gonad (testis) causes female characteristics.

Implantation

-Day 0 > fertilization -Day 7-10 > implantation in uterine wall -Blastocyst: outer cell layers of cells which separate outside world from the blastocele (inner cells) is call trophoblast. Inside, there is inner cell mass at one end of blastocyst -binding on the endometrium is by syncytial (sin-sish-ul) trophoblast) -fingerlike vili extends away from trophoblast into endometrium and the inner cell mass separates forming the amniotic cavity

Cervical Cancer

-Dysplastic changes in the cervical mucosa: A. Benign: cervical Intraepithelial neoplasia (CIN) B. Maliginant: 80% squamous cell carcinoma, 20% adenocarcionma. -Adenocarcinoma: is less common and is much harder to dx bc its deep in the cervix and missed by regular CST. Epi: Cervical intraepithelial neoplasia (CIN): 2%: common Cervical cancer: RARE > 0.2%. 4th most common cause of cancer related mortality in women and the most common in teh developing world. RFs' 1. Sexually active: multiple sexual partners (sophie) 2. Age: 40-50: peaks in women aged 40-50 mainly bc of the delayed process between exposure and development of disease 3. Multiparity 4. Immuno suppression 5. smoking: increased risk of squamous cell carcinoma but not adenocarcionma Etiology: -HPV 16 and 18 > cervical cancer -HPV 6 and 11 causes genital warts -peak infection incidence is late teens and early 20s *in 80% of pts the infection resolves within 12-18 months: once infection resolves > risk of cervical cancer returns to baseline. -Transmission: via mucosal secretions of the genital tract as well as secondary objects (dildos) Pathophys: -uterus: glandular columnar epithelium -Vagina: squamous epithelium -Transitional zone: at puberty > get eversion of endocervical mucosa > columnar epithelial cells move out of canal of cervix and form the transition zone > transition from columnar to squamous Hx: 1. Asymptomatic 2. Intermentrual spotting: occurs between periods 3. Post coital bleeding 4. Vaginal discharge: clear and less smelly than PID Red flags: 5. Bone pain 6. Bladder, renal or bowel obstruction HPV 16 and 18 have potential to induce dysplastic mutations within this transitional zone. Cervical intraepithelial neoplasia: grades: CIN 1: low grade dysplasia, partial epithelial involvement. Grade 1: low grade (mild dysplasia or low grade SIL) CIN 2: extend through epithelium: high grade or moderate dysplasia or high grade SIL CIN 3: carcinoma in-situ (premalignant): high grade, severe dysplasia/CIS or high grade SIL (squamous intraepithelial lesion) Cervical squamous cell carcinoma: transition from CIN to malignancy is 15-20 years!!! -This is why we changed from 2 to every 5 years CST bc the cancer takes a long time to progress. Peak infection is late teens to 25 > peak incidence of Cervical squamous cell carcinoma is 40-50s

7 cardinal movements of labour: Every Day fine infants enter eager and excited

-Engagement, Descent, Flexion, Internal rotation, Extension, external rotation (restitution: spontaneous realignment of head w/ shoulders), explusion Attitude: position of babies joints: normal labor > begins w/ all joins in flexion. Sub occipito bregmatic: is 9.5cm >> smallest diameter. Sub mento bregmatic: 9.5cm 0occipitofrontal: 11.5cm Occipitomental: 13.5.

Infection

-F/R/N, confusion PLUS: 1. Post partum Endometritis: -commonly caused by Strep agalacticae (GBS) or colorectal flora that ascend > infection of endometrium. Most often the placenal bed -Look for: A. Increased white or smelly lochia B. Suprapubic pain 2. UTI: FTs: -abnormal dysuria (Storage FUND) -pyuria: pus 3. Mastitits: -skin commensal (staph aureus) infection of lactiferous ducts Fts: -painful, red swollen lobule in the breast 4. Wound infections: -CS wound infections r more common in obese women w/ an apron. FTs: -wound discharge, redness, swelling, lack of adhesion 5. IV or catheter infection Ix: -Urinary MCS -Swab of infectio nsite -vital signs -FBE, blood culture, CRP/ESR Mx: -endometritis: refer to hospital > IV antibiotics (clindamycin and gentamycin until afebrile for >24 hours).

Methotrexate contraindications

-hemodynamic instability -bHCG >5,000 -Poor compliance bc regular BHCG follow up is needed to watch down trending Salpingectomy: removal of ovarian tubes > low rx of recurrence bc u have infertility now Salpingotomy: excision and repair of tube > maintain fertility but ^ rx of recurrence. Monitor BHCG until 0.

Risk of spinal and epidural anesthesia

-infection -damage to local structures > paralysis -hypotension and hyperthermia may result but often mild -slows progres of labor: both 1st and second stage (+1 hour) -^ rx of instrumental delivery Contraindications: -overlying infection -coagulopathy: platelets <75, any anticoagulants -hx of spinal surgery -allery to local anesthetics or opiods

Vasa Previa:

-Fetal blood vessels cross or near the cervical os -risk of rupture when the supporting membranes rupture, as they are unsupported by the umbilical cord or placental tissue. Arises from 2 major abnormalities of placenta: 1. Velementous cord insertion: instead of cord passing from baby directly into the placenta , the umbilical cord inserts into the amniotic membranes just next to the placenta. Vessels travel btwn external chorion and amnion into the placenta. 2. Bi lobed placenta: -when these free vessels sit low in uterus > rupture either during SROM (spontaenous rupture of membranes) or ARM (artificial rupture of membranes) causing severe fetal hemorrhage. *neonatal mortality >70% bc the vessels rupture contain fetal blood!!!! Epi: rare -not only do u need to have these abnormalities, u also need to be low lying placenta to allow rupture. RFs: -previous cesarean section -smoking Hx: -asymptomatic - hemorrhage then fetal death very quickly -bleeding on ROM -Non painful Ix: -ultrasound: must look for vasa previa in low lying placenta at 30 weeks or in velamentous cord insertion/bilobed placenta -CTG: sinusoidal trace > severe fetal anemia Mx -Cesarean: dont want membranes to rupture. Deliver to avoid cxs of rupturing membranes and vulnerable vessels of the baby.

Depot Provera (progesterone only injection): every 3 months

-IM depot of medroxyprogesterone acetate -supresses LH > thickens mucus and thins endometrium Given: every 3 months by GP or self administer Benefits: 1. Can be done with nurse or self admin 2. 70% get amenorrhea Cons: 1. Menorrhagia: heavy/prologed periods 2. Weight gain 3. Headache, N, depressin bloating, anxiety 4. contraception effects may persist for 12 months after cessation

Cervical screening test:

-If negative for HPV > then repeat test in 5 years -If HPV 16/18 detected > Liquid based cytology > colposcopy -If HPV non 16/18 detected > liquid based cytology > if negative for HPV or positive > repeat after 12 months. After 12 months if positive > LBC > if poistive for cervical dysplasia> colposcopy. if negative > do it after 5 years . Confirmed high grade cervical intraepithelial neoplasia: 1. Large loop excision of the transitional zone (LLETZ) or cone biopsy: A. LLETZ: premenopausal or child bearing: under General anesthetic > loop diathermy is used to remove transitional zone of cervix and ssent for histology. B. Cone biopsy: post menopausal women: large piece of tissue is taken from cervix.

Women infertility

-Inability to conceieve after 12 monthhs of unprotected sex -Epi: 6%: Aetiology: -cervical/uterine abnormality -tubal disease: primary cause worldwide is due to infection > gonorrhea, chlamyida, tuberclosis. -ovulatory dysfunction >> MOST COMMON cuase and is due to age. Decrease accelerates at age of 35. Also due to PCOS (5% women). Also high or low BMI is related to ovulatory dysfunction -unexplained infertility -cigarettte smoking Pathophys: -ovulatory dysfunction: A. Hypogonadotrophic anovulation occurs due to hypothalamic/pituitary abnormalities: ^/low BMI, heavy exercise/diet, stress, sheehan's syndrome, prolactinoma > hyperprolactinemia > inhibit GNRH (low fsh/lh) B. Hypergonadotrophic anovulation occurs as a result of ovarian failure (congenital/FHx of early menopause, fibroid, polyp, synaechia (fibrous adhesions form > ashermans syndrome), PID, perforated appendix, endometriosis. C. Eugonadotrophic anovulation is most commonly due to PCOS. -tubal disease: most caused by gonorrhea and chlamydia > cause salpingitis (inflammation of fallopian tubes) > 10% risk of tubal occlusion. -Any Pelvic infection including appendicitis and diverticulitis can damage fallopian tubes -endometriosis > growth of hormonally responsive endometrial tissue outside of uterus > may obstruct fallopian tubes -age related > decline in oocyte number and poor quality. -unexplained: failure to conceve after 2 years of UPSI -uterine abnormalitiies: conggenital or acquired. Leiomyata can cause tubal obstruction. -cervical surgery/infection RF's 1. >35: chance of preg decreases by 5% every year over 30 years. 2. Hx of STD: chlamydia and gonorrhea affect fertility by cauisng damage to genital anatomy. -chlamydia: intracellular parasite > invades cervix, uterus, tubues > can cause tuubeo-ovarian abscess. Chlamydia can be asymptomatic in 75% of cases 3. Very low BMI or high BMI/PCOS: In PCOS > u have hyperinsulinemia and overproduction of androgens >infertility 4. Cigarrete smoking: accelerates follicular apoptosis and earlier menopause. Hx: 1. RFs 2. Hx of pelvic surgery (myomectomy, ovarian cystectomy or others) 3. Irregular period: normal cycle is 24 to 35 days w/ bleeding for 3-7 days. 4. Hirsutism: midline abdominal or male pattern hair growth 5. Acne 6. Palpable uterine abnormalities (shape and mobility of uterus) >> fibroids/scarring from endometriosis 7. Adnexal massess/tenderness indicating endometriosis/infection 8. Galactorrhea: common sign of elevated prolactin. Leads to amenorrhea

Pelvic Inflammatory Disease (PID): CAMAr Dard: Ceftriaxone, Azith, Metronidazole (14 days), plus Azith/doxy a week later

-Inflammatory disorder of female upper genital tract and includes: Any combination of: ovaries (oophoritis), fallopian tubes (salpingitis, tubo-ovarian abscess), uterus (endometritisi), pelvic peritonitis -Sxms: fever, vomitting, back pain, dyspareunia, bilateral lower abdo pain, odour, itch, bleeding, d/c Epi: 1 million women each year in US. Most common gyne condition -occurs in sexually active women w/ Hx of STD -peaks in women 20-24 yrs Aetiology: -STI related 85%: Neisseria gonorrhea, chlamydia trachomatis, Mycoplasma genitalium -Non STI related (normal flora): Hemophilus vaginalis, H. Influenza, strep agalactiae (Group B, Beta Hemolytic strep: GBS), mycoplasma homini, ureaplasma urealyticum *60% is asymptomatic Clinical case definition: due to asendign spread of oragnisms to upper genital tract: -All of the follow must be present: 1. Abdominal tenderness 2. Tenderness with motion of cervix 3. Adnexal tenderness (appendages of uterus > tubes, ovaries, ligaments AND atleast one of the following: 1. Temp > 38 2. D/C 3. Elevated ESR or CRP or WCC 4. N. gono or chlamydia positive on culture or histology (endometrial biopsy) 5. Radiological abnormlaities 6. Pelvic abscess Pathophys: -infection begins in cervix > if untreated > ascend to upper genital tract. -Epithelial damage caused by N. Gonorrhea and chlamydia trachomatis > allow entery of other microorganisms. -can also be caused by intrumentation of cervix such as D&C, termination of pregnancy, or insertion of IUD. -Infection > caused by disruption of cervical barrier and direct introductio nof bacteria into endometrial cavity. RFs: 1. PHx of chlamydia or gonorrhea: most important risk factor!!! 2. Young age of sexual activity 3. Unprotected sex with many partners 4. PHx of PID: impaired local host defenses 5. IUD use: within first 3 weeks after insertion 6. Smoking 7. Current vaginal douching: alterns normal flora, causes epithelial damage and disrupts cervical mucus barrier 8. Sex during menstruation Hx: -RFs -uterine tenderness -cervical motion tenderness -lower abdo pain -mucupurulent discharge -fever, N/V Fts: Gonorrrhea: Less common in women but symptomatic. More common in men (75%) Gram neg -acute -may have temp >38 -cervicitis -discharge common WCC and ESR elevated Chlamydia: more common in women (75% in women 15-29). A/w reactive arthritis* get sacroiliatis Gram neg -Subacute -temp <38 -cervical tenderness -varying degree of cervicitis -WCC is lower, ESR is normal -**75% is asymptomatic Ix: 1. B HCG: exclude preg 2. FPU, cervical/ vaginal swab: chlamydia, N gono PCR 3. Endocervical swab > culture 4. FBE: WCC 5. CRP and ESR: ESR will be elevated 6. Blood cultures if sepsis 7. STI screen: serum serology for HIV, syphilis, hep b and c 8. Pelvic ultrasound first line 9. Laparoscopy ******if NO CERVICAL discharge + NO WBCs on wet prep = PID unlikely ***** Mx: stat means immediately: Dont ****ing have sexual contact: drugs, fact sheet, health department, no sex for 7 days, contact tracing. Sexually aquired: CAMA or Dard: -mild to moderate > outpt + oral AB's: Ceftriaxone 500mg IM stat + Azithromycin 1g stat + metronidazole 400 mg BD (14 days) plus azithromycin 1g stat one week later or doxycycline 100mg BD (14 days) -Severe infection (Admit + IV ABs: ceftriaxone 1g IV + Azithromycin 500mg IV + metronidazole 500mg IV BD then chagne to amoxycillin/clavulanic acid + doxycycline to complete 14 days. -partner notification and treatment -Notify health department : make sure pt knows that u have to report the case if its an STI: initials and the post code: just for tracking (Chalmydia > Azith. Gonorrhea: Azith + Cef. Aneroes > Metronid, Gram negatives > doxycycline) -Follow up Non sexually acquired: -mild-moderate: amoxycyllin/clavulanate bd 14 days + Azithromycin 1g plus azithromycin 1g 1 week later or Doxycycline 100mg bd 14 days *ony need to take a mirena out if its <3 weeks since insertion Cx's: -10% ectopic pregnancy -20% chronic pelvic pain -20% infertile- chalmydia and gornorrea damage epithelial of reproductive tract > form adhesions > infertility and tubal ectopic -Tubo-ovarian abscess or pelvic aabscess: serious life threatening condition > require emergency surgical intervention. Pelvic abscess arises wen bacteria leave the ovarian tube and collec in peritoneal cavity. Sxms: pelvic mass, positive leg raise and obturator signs -systemic infection > infect other organs or septic shock -Fitz-Hugh curtis syndrome: RUQ abdo pain representing perihepatitis > "violin string" BUZZfibrous scar tissue (adhesions) between the liver and the abdominal wall or the diaphragm Delay in tx >48 hours > 3X increased risk of ectopic preganncy, infertility Repeated episodes: 6X risk permanent tubal damage.

Ovulation cycle:

-Kisspeptin: produced in hypothalamus > control production of GNRH: gonadotropin releasing hormone > induces ovulation. -Leptin: produced by fat cells stimulate pituitary to release LH > induce ovulation. Gonadotropin Releasing Hormone: controls release of gonadotroic hormones FSH and LH -production occurs in pulsatile fashion. A. Slow: stimulates production of FSH from anterior pituitary. (S for slow) B. Fast > stimulates production of LH from anterior pituitary -GnRH is released from hypothal > hypothalamic hypophysial portal system to anterior pituitary > FSH and LH release.

Shoulder dystocia: ALARMER

-Occurs during second stage of labour> there is delivery of head but the shoulders become impacted on the margins of pelvic outlet. Signs include retraction of babys head back into the vaina known as "turtle sign" Cxs for baby: brachial plexus injury, clavicle fracture, Erbs palsy (Waiters tip position: x upper brachial plexus C5/6: X innervation to deltoid, bicep and brachioradialis>> shoulder adduction+elbow extension+pronation), klumpke paralysis (damage to lower brachial plexus C8, T1), fetal hypoxia/detah, cerebral palsy Cxs for mom: vaginal or perineal tears, PPH or uterine rupture Pathophys: anterior shoulder becomes impacted on the pubic symphysis (majority) or the posterior shoulder on the sacral promontory Aetiology: ^ shoulder: head ratio or a small fetal head RFS: -gestational diabetes: 2-4 fold increase in rx -Phx of shoulder dystocia -obesity: ^rx of GDM -macrosomic baby: >4.5kg -epidural anesthesia ->35 yo - short stature ->4.5 kg Factors that ^ rx: -prolonged first and second stage of labour -turtle sign: head retracting -failure to resitute -instrumental delivery Diagnosed when body fails to deliver within one minute of delivery of baby's head. It is a type of obstructed labour Aetiology: -macrosomic baby , head circumference >90th centile > potential cause of cephalopelvic disproportion -transverse lie, breech or deflexed vertex, occiput posterior positions Hx: Slow progress: -active stage 1: primi >1cm/hr, multi >1.5cm/hr -stage 2: primi >2 hours, multi >1 hour : +1 hr if on epidural -maternal tachycardia and pyrexia: -macroscopic hematuria -fetal tachycardia on CTG -Bandl's ring (retraction ring): m shape abdomen > obstructed labour. ALARMER -Ask for help: Both obs and peds, + IV Benpen 2 doses >4 hours apart when membranes r ruptured >18 hours. -Leg hyperflexion and abduction at hips (McRoberts manuever) -Anterior shoulder disimpaction (suprapubic pressure) -Rotation of shoulder (Rubin manuver) -Manual delivery of posterior arm -Episiotomy -Roll over on all fours *if all of the above fails: 1. Cleidotomy: most common: clavicle of baby is broken to allow delivery 2. Symphisotomy: dissection of pubic symphasis 3. Zavanelli and Cesarean: performed when fetal head can be pushed back (Zaavanelli manuever) into the vagina and there is no signs of cord compression. **Must 1. Document 2. Debrief family 3. Depression > monitor for PND

Miscarriage:

-Pregnancy loss prior to 20 weeks -Early pregnancy bleeding is defined as bleeding before 20 weeks gestation -20% of preg women will have some bleeding before 20 weeks. -synonymous w/ abortion Epi: 1 in 5 pregnancies will miscarry -I know this doesnt take any grief away but u are not alone and that many women understand what u r going through. 1 in 5 pregnancies will end in a miscarriage. Aetiology: majority of miscarriages occur in 1st trimester w/ <3% occuring in second trimester. 1. 80% of first trimester miscarriages is due to > CHROMOSOMAL ABNORMALITY > MOST COMMON CAUSE: spontaneous mutations w/in embryo developed during replication 2. Embryonic malformations 3. bacterial vaginosis > a/w second trimester miscarriages 4. Large sub mucosal fibroids compromise early embryonic angiogenesis 5. Antiphospholipid antibody syndrome: 1st and 2nd trimester recurrent miscarriage. 6. Herbs: aloe vera, karela (biter melon), celery *Most common causes of 2nd trimester miscarriages r cervical incompetence, weakness or insufficiency following invasive fetal dx procedures;transplacental fetal viral/bacterial infection, rhesus isoimmunisation. Pathophys: -vaginal bleeding occurs from decidual implantation site or from placenta > lead to hypoxic or vascular causes > lead to placental dysfunction >> fetal demise/death Categories: Only i ones are d"i" lated cervix > incocmplete and inevitable. M for minimal bleeding/brown stain > Missed. 1. Biochemical pregancy: -preg not located on scan, rise in BHCG and rapid fall, level not high enough to see sac on US, late period 2. Spontaenous miscarriage: spontaneous expulsion of products of conception. Presents as bleeding during early preg usually w/ pain 3. Complete miscarriage: uterine cavity emptied all POC (empty on US) => Conservative Mx: paracetamol, counseling, psychiatric support, anti-d in RH- mom. 3.1 Incomplete miscariage: vaginal bleed, cervical dilation, incomplete POC, No HR: Mx: paracetamol, counsel, info, psychiatric suport, misoprostol, 4. Missed miscarriage : retention of POC w/ little/no bleeding/brown vaginal discharge. Uterus is small for dates. Tx: D&C, medical (methotrexate) or expectant (waitful watching). -US >non viable preg 5. Threatened miscarriage: Tx: paracetamol for pain, avoid NSAIDS, anti D if RH -, counsel, follow up w/ fetal surveillance. Spont vaginal bleed in first half of preg have uneventful pregnancies thereafter. -fetus heart sound present -vaginal bleeding -closed cervix -threat of miscarriage exists when vaginal bleeding w/ or w/or abdo pain occurs in preg of 20-24 weeks and where preg may continue. -if US shows fetal Heart sound after vaginal bleeding > 90% chance pregnancy will progress. Tx: conservative mx 6. Inevitable miscarriage: (cervical shock: POC or clots i nopen cervical os > pt has Low HR and Low BP: Tx by removing POC from os) -when cervix is open > POC protrudes into vagina. -preg will not continue and will proceed to incomplete or complete miscarriage. -vaginal bleeding -POC in uterus, need to be expelled Tx: conservative mx or active (removal of products w/ or w/o general anesthetic. -manual evacuation digitally or forceps, paracetamol for pain, avoid NSAIDS, counsel, psychiatric support, low chance of miscarriage should be mentioned if any worry is expressed about future. -those who continue to bleed after manual evac > get misoprostol > aid in complete emptying of uterine cavity -antid in Rh- mom 7. Recurrent miscarriage: spontaneous loss of 3 or more consecutive pregnancies before 20-24 weeks - 1 in 5 w/ a hx of recurrent miscarrriage may have further preg loss. -pts w/ antiphospholipid syndrome or inherited thrombophilias have been txed w/ low dose aspirin started before conception > may need heparin therapy after positive preg test until delivery. -counsel -info -psychiatric support 8. Septic abortion: occurs in those a/w retained POC > threatened, missed, inevitable, incomplete -vaginal discharge, vaginal smell, abdo pain, F/R/N -Cxs: septic shock: fever, hypoten, tachy, DIC, multiorgan failure Dx: -no fetal heart on US after 6-7 weeks -expect gestational sac 25mm -falling B HCG levels RFs: -older age >45 yrs -uterine malformation (congenital-> unicornuate or bicornuate uterus a/w cervical weakness/incompetence or acquired -> sub mucus fibroids) -bacterial vaginosis: important role in second trimester miscarriage and preterm delivery -thrombophilia: hyperhomocysteinemia is rf for recurrent miscarriage: presence of anti-cardiolipin antibodies (Antiphospholipid Syndrome APS-> anti-cardiolipin antibodies and lupus anticoagulant > >autoimmune disease that increases clot formation and miscarriage) carries 9X risk of fetal loss -parental chromosomal anomaly: robertsonian translocation -Previous spontaneous/induced miscarriage -IVF -NSAIDS and Caffeine: 100mg caffiene/day a/w 7% higher rx of preg loss. -OH and smoking -obesity -hypothyroidism and diabetes mellitis (high HBA1C > ^ rx of miscarriage and fetal malformation due to toxic metabolites) -Systemic Lupus Errythematosus: in SLE > a set of auto antibodies can arise in addition to the Anti dsDNA and ANA. Predisposes to intravascular thrombosis > miscarrage: antibodies include: DX of APS: 2 positive tests 12 weeks apart + LA or Anticardiolipin antiodies IgG and or IgM A. anti-cardiolipin antibody B. Anti B2GP1 C. Lupus anticoagulant Tx: low dose aspirin plus heparin to prevent further miscarriage. Heparin doesnt cross placenta. Hx: -rfs -vaginal bleeding w/ or w/o clots -suprapubic pain -low back pain -post coital bleed: odds of miscarriage doubles who report bleeding after sex during pregnancy -uterine struc abnormalities: sub mucus fibroids co-existing w/ ongoing pregnancy may increase rx of bleedign in early preg **Make sure you ask if pt has ASTHMA > need to avoid medical mx (MISOPROSTOL) Ix: -high vaginal swab > asymptomatic bacterial vaginosis ^ rx of miscarriage -urine BHCG: doubles every 2 days in first 10 weeks. <5: not preg. 1,500 > gestational sac on US. 10,000 fetal HR -FBE: low Hb due to blood loss -blood group and hold -Coagulation studies: thrombophilia: decreased clotting time -Rh group: anti-d in Rh - mom -serum BHCG: falling levels > failing preg: drop in >50% in 2 days is > failing preg -transvaginal ultrasound: when gestational sac >25mm > should be a yolk sac or fetal pole present. Crown rump length: >7mm > fetal heart -SLE screen: in pts w/ recurring miscarriage 3 or more miscarrages. DDX: -ectopic: adnexal tenderness, suprapubic pain, pallor, tachycardia, syncope -hydatidiform mole: uterine size is larger than for gestational age, , passed grape like tissue -cystitis (bladder infection: suprapubic pain,fever,hematuria dysuria > do urine MCS -cervical polyp - ectropion: glandular uterine cells spread to outside of cervix Complications: -incomplete evacuation of POC -post evac bleeding -sepsis: occur before or after miscarrage: fever/chills/ abdo pain -uterine/cervix perforation -recurrent miscarrage: affects 1-2% -asherman's syndrome: follows curettage w/ trauma to endometrial lining > results in uterine cavity adhesions > obliterate the cavity > result in infertility, recurrent miscarriages and high risk preg. -psychological dysf Mx: -expectant: watch and wait: wait for uterus to expel POC naturally. Rx: may take upto 4 weeks and is a/w ^'ed bleeding and septic cxs -medical: misoprostol: 2 doses 12 hours apart. PV prostaglandin (PE1) used to contract uterus and help expulsion of POC A/e: cramping, N/diarrhea, blood loss. Best for incomplete or missed miscarriages. Takes 3-8 days. -Surgical: Cervical dilation and suction currete (D&C). A/e: bleeding, cramping. Risks: anesthetic rsk, intro to infection, damage to uterus -in everyone: 1. Treatment of anemia: Fe supplementation or blood transfusion 2. Blood group and Anti D: in Rh - mom. <12 weeks: 25IU >12 weeks give 625IU Expectant: threatened, missed, inevitable, incomplete, complete Medical: missed, inevitable, incomplete Surgical: missed, inevitable, incomplete, SEPTIC + -Weekly monitoring until bleeding settles -Septic > broad spectrum antibiotics.

Bleeding in early pregnancy

-Prevaginal bleeding <20 weeks gestation > threatened miscarriage. Epi: 1 in 5 pregnancies will miscarry thus bleeding in early pregnancy is really common but 1% of these will be an ectopic and smaller proportion will be gestational trophoblastic disease GTD. Aetiology: -extrauterine: ectopic pregnancy -intrauterine: miscarriage or gestational tropholastic disease GTD -lower genital tract: incidental bleeding Hx: -GPA -Cxs -blood group -pregnancy sxms: amenorrhea, N/V, breast tenderness -when did bleeding start and has it always been the same? -when did u notice it? -qaulity: appearance? Fresh or darker and clotted? -quantitiy? Soaking through 1 pad an hour? -lightheaded, palpitation, dizzy? > anemia DDX: 1. Ectopic: pale, sweating, pain, lying still > peritonitis -severe lower abdo pain -light headed/dizzy -Hx of PID or STI, IUD or progesterone contraceptives 2. Miscarriage: -vag bleeding -passage of products? -large clots? -lower pelvic cramping rather than constant pain +/- back pain -F/R/N =Speculum and transvaginal ultrasound needed 3. Gestational Trophoblastic disease GTD: -vaginal bleeding during preg -hyperemesis gravidarum: severe Nausea and vomitting during pregnancy -early onset pre-eclampsia: headache and/or swelling of hands and feet. -fts of hyperthyroidism: heat intolernace -vaginal passage of grape like cysts -hemoptysis or pleuritic pain 4. Incidental bleeding: -post coital -post exam or recent pap smear clear? -dark and small in volume Exam: General well being: ectopic pt > very distressed lying still in pain Vitals: -hemodynamic instability > ectopic rupture -bradycardia > presence of retained products in cervix -febrile+tachy > septic abortion and infection Abdo exam: Palpation: -hard, rigid abdo +++ garuding > ectopic preg -tender on palpation, crampy pain in pelvis/bakc > miscarriage -larger than expected uterus > Gestational trophoblastic disease GTD Speculum exam: -POC > incomplete miscarriage -Open cervix > incomplete/complete miscarriage -D/C: infection -lesions, polyps, trauma > incidental bleeds Bimanual vag exam: -cervical motion tenderness > infection or septic abortion -adnexal mass > ectopic -Large uterus > GTD Ix: -FPU for STI -urinary B-HCG -serum b hcg: doubles every 48 hours in first 10 weeks until it reaches 50,000 then drops ut remains elevated until delivery A. <5 > not preg B. 1,500 > gestational sac on US C. 10,000 > should see fetal heart rate -FBE, group and hold, coagulation studies, -kleiheur or KB test: assess amount of fetal maternal hemorrhage and thus how much anti D is given. In all RH- moms > need to give anti D to prevent antibodies from building. -Transvaginal pelvic ultrasound

Lactation

-Prog and est promote development of anatomical mamary system -milk production > controlled by Prolactin from posterior pituitary gland -Estrogen and progesterone cause Negative feedback on prolactin secretion before delivery meaning > no milk is produced. Galactopoesis: -decline in estrogen and progesterone following delivery > prolactin is released > stim production of milk within alveoli post partum -initial milk: colostrum: A. 0.5 -> 5ml -high in immunoglobulin's and some fat >> energy is low thus babies weight often drops over first few days. Mature milk > lactogenesis: -progressively larger volumes > report feeling fullness of breast > around day 4. -^ carbs (lactose), fats, nutrients, and hormones which match babies needs -carbs within the mature breast milk follows after 1 week > babies weight increases Components of breast milk: 1. Water 2. Faats 3. Sugars 4. Antibodies 5. Hormones: A. TSH > stimulates fetal thyroid to producce thyroxin B. Prostaglandins > aid neonatal peristalsis and protect the fetal gut from inflam C. Cortisol > promotes fetal development as a whole. D. Epidermal Growth Factor > promotes fetal growth and development particularly the gut and production of lactase enzymes required to use breast milk lactose. Protective against lactose intolerance How long? -exclusive breast feeding: rec upto 6 months of age w/ continued breastfeeding along with appropriate complementary foods upto two years of age or beyond. How often? 1. On demand: whenever baby desires 2. 8-12 times a day: 3. Every 2 hours. Reflexes: 1. Ejection of milk > let down reflex: -milk produced > in mamary glands > stored and secreted by glandular cells lining the alveoli > stimulation > > ejecection -baby sucks > stim production and release of oxytocin from posterior pituitiary gland > stimulates contraction of myoendothelium > ejection of milk into lactiferous sinuses 2. Prolactin adjustment: i want more reflex -suckling stimulation causes inhibition of prolactin inhibitory hormone in hypothalamous (its a double negative: low inhibition means more stimulation of prolactin) -greater stimulation > ^er prolactin release Poor milk let down: sheehans syndrome: -due to high metabolic demand of post pituitary during labour (^ oxytocin) > cells r predisposed to metabolic strain >> PPH > hypoxia >> infarction >>leads to no prolactin and no let down of milk. *have lobules containing acini (site of milk formation: have myoepithelial cells around epithelial cells) >ducts > lactiferous duct > lactiferous sinus > nipple > site of milk expression. ********** Prolactin stimulates production of milk Oxytoicn stimulates contraction of myoepthielial cells >>milk ejection

Bishop score <8: must do cervical ripening: Prostaglandins and Foley balloon catheter

-Prostin gel: Prostaglandin E2: gel form > inserted into posterior fornix to promote ripening (cause uterine contractions) -Cervadil pessary: PGE2 in a pessary form > safer bc we reduce rx of hyperstimulating uterus if gel gets into endocervix or uterus. -Misoprostol: oral 200mcg PGE2: mainly used in First (miscarriage) or second trimester induction because of hyper stimulation in T3. Risk: unlikely: -uterine hyperstimulation w/ prostin gel > hypoxic effect on fetus -hypertonic uterus can also cause placental abruption -GI upset *Grand multiparity (P5) and uterine scar r major CI for prostaglandin ripening > predispose uterine rupture Benefits: comfortable while waiting for labour, quick, effective Foley balloon catheter: 30ml foley ballooon catheter passed through cervix > inflated w/ saline in lower segment of uterus and rested on internal os > physical pressure of balloon > ripening. -foley balloon is usually expelled from lower uterine segment through the cervix overnight, leaving a cervix ripe for induction of labour the next morning. rx: Infection: very nare, discomfort over night, slower Benefits: -non pharma -reduce rx of hyperstimulation -cost effective -preferred method for VBAC bc we dont want to give prostaglandins to a women w/ a scar -use thi sin multiparous women ******good thing about both of these is tat an ARM or oxytocin induction may not be required bc both of these agents may stiulate labour by themselves.

Normal Puerperium

-Puerperium, the period of adjustment after childbirth during which the mother's reproductive system returns to its normal prepregnant state. It generally lasts six to eight weeks and ends with the first ovulation and the return of normal menstruation. -if pt breastfeeds > most get period 9-18 months later. Lochia: uterine discharge arising from site of placenta detachment and may last upto 8 weeks. -uterine vasculature that passes through myometrium to endometrium is left exposed on detachment of placenta > contraction of myomet allows ligation of these vessels. This site needs to heal. 3 stages: 1. Lochia rubra (red color) is first discharge (blood,shreds of membrane,decidua) - lasts 3-5 days after birth 2. Lochia serosa (Pink/Brown color): lochia that has thinned and turned brownish/pink in color: 5 days. If lasts for weeks > indicate late PPH 3. Lochia alba (whitish/yellowish-white): last upto 6 weeks after delivery. Beyond this time > > genital lesion. Amenorrhea: -production of prolactin from post pituitary suppresses folliculogenesis thus suppression of estrogen production and the development of endometrium. -Normal menstration and fertility return 6 weeks post partum. -contraception is important discussion before discharge home Contraction of myometrium: -takes 6-8 weeks for uterus to shrink back to normal size Urogenital atrophy: dryness and dyspareunia -same mechanism as menopause > low levels of estrogen > bc of suppression of folliculogenesis >> dryness of vagina and cervix. -if need colposcopy after detecting CIN in antenatal scan > wait 6-8 weeks for estrogen to return. Pelvic floor weakness: may get minor incontinence >>> need physio referral for pelvic floor strengthening. Post partum strain: slight ^ in cardiac demand immeidately after delivery due to loss of placenta. Worry if pt has CVD, valvular stenosis. Reduction in swelling > peripheral vasoconstriction >>excess fluid removed Urinary retention: fail to pass urine after 6 hrs following NVD or removal of catheter. -common after CS, epidural, prolonged labor. Hematuria: may haev minor damage to urethra during NVD. Should resolve w/in 24 hrs. Constipation: due to opiate analgesia (pethedine) Resolution of insulin resistance: DONT continue insulin Resolution of breathlessness. Retained or new SOB >> DVT/PE, cardiac insufficiency, anemia, and asthma Resolution of immune deficiency: Can flare in autoimmune disease: MS, Graves disease, Hashimotos -can get vaccinations post partum Hypercoaguability: -pelvic veins r engorged w/ blood > ^ rx of thrombosis > check calves and thighs for DVT >> important part of post natal exam. Anemia: -blood loss during pregnancy or PPH >>microcytic (when prolonged bleeding) or normocytic (PPH) anemia. -supplement w/ Fe > Ferograde C.

Placenta Accreta: Adhesive disorder of placenta: non painful bleeding, no tenderness/contraction

-adherence of placenta to myometrium rather than the thickened endometrium Terms: occurs due to loss of endometrium -accreta (75%): invasion below endometrium > on myometrium. -increta (17%): in the myomtrium -percreta (5%): placenta protrudes through uterine wall and involve other structures (bladder) Epi: 1 in 2,500 Cxs: -death and sadness -adhesion to myometrium result in lack of normal separation at delivery leading to marked hemorrhage > needing emergency hysterectomy -ofte nfatal to both mother and baby bc of such high vascularity RFs -previous cesarean section -Placenta previa -age >35 **risk of Accreta increases with number of cesearean sections! Hx: -painless PV bleeding -previuos cesarean section: bc theres a big scar > placenta can imgrate deep into the myometrium. Ix: -low lying anterior placenta on 20w ultrasound- bc previous Cesarean is biggest risk factor >majority of placenta accreta arises in ANTERIOR part of lower segment of uterus. Mx: -resuscitate mother with saline -Mom: DRS ABC: -baby: CTG -resus: blood group cross match, saline -cesarean section + hysterectomy due to the severe blood loss

Chorioamnionitis (Uterus)

-bacterial infection or inflammation of the fetal amniotic and chorionic membranes Routes of infection: 1. Ascend from vagina 2. Amniocentesis 3. Hematogenously via placenta (listeria) 4. Retrograde from abdominal cavity -normal vag flora: mixed aerobes and anaerobes (mainly lactobaccilus or BS) -interconcurrent disease: STIs -listeria: most common transplacental cause of chorioamnionitis EPi: -9.7 per 1000 live births Aetiology: When protective mechanisms of urogenital tract or uterus fails or when ^ed number of microbial flora or pathogensic microorganisms r introduced. Ascends into vagina > cervix > uterine cavity > fetal membranes and placenta Pathophys: ascending of vaginal flor through cervical canal is most common pathway to chorioamnionitis. -can occur via hematogenous spread (listeria) or via contaminaitaon of amniotic cavity (amniocentesis) RFs: -Longer durationtn of membrane rupture -PPROM: major rx factor > need to give erythromycin TDS for 10 days -prolonged labour -nullparity -multiple vaginal exams -meconium stained amniotic fluid -smoking, OH, immunocompromised Hx: -uterine tenderness -pale grey smelly d/c -maternal fever and tachy -CTG; fetal tachy Ix: -high vaginal swab > vaginal flora -FPU > STI's -FBE > sign of infection -CTG: fetal tachy Consequences: -dx warrants asap AB and delivery of baby bc of very serious rx to maternal and fetal well being. Mx: -admit and stabilize + IV access + call for help -Triple antibiotic therapy: normal flor or STI's thus cover the 3 arms of infection: 1. Gram positive > ampicillin 2gIV 6hrly 2. Gram negative > gentamycin 6g IV daily 3. Anaerobes > metronidazole 500mg 8 hourly

Rupture of membranes without labour

-before labour starts but term >> Premature rupture of membranes PROM -before labour starts pre-term >>Preterm premature rupture of membranes PPROM PROM: -membranes rupture after term but there is no transition into labour. -decide if u want to induce now or wait a little bit and risk infection Pre-term Premature Rupture of Membranes: -membranes rupture <37w -leading cause of pre-term labour and pre-term birth involved in 1/3 of cases Spontaneous rupture of membranes SROM: -term gestation: rupture of membranes started by normal laboring contractions of uterus. Epi: -Rupture of membranes is a big part of stimulating the normal labour but it does not occur the same way in all women. -Normally, contractions occur, then get rupture of membranes. -Rupture before labour (contractions) begins —> 10% -Rupture just before stage 2 —> 25% -PPROM —> 3% of pregnancies • PROM: water breaks (Prelabour rupture of membranes) > complications of prematurity • Causes: ○ Prom: § 10% of all preg § 30% of prom are preterm (PPROM) ○ Causes: § Infection: bacterial □ BV, chalmydia, GBS, E. Coli, mixed □ Develops early chorioamnionitis § Labour □ Cervix already ripened □ a/w recurrent bleeding □ Usually go into early spontaneous labor § Idiopathic. • Complications: ○ Term prom: § Fetal/maternal infection □ Chorioamnionitis: severe maternal sepsis □ Post partum endometritis § Cord prolapse ○ PPROM § Same as above § + preterm labour/prematurity ○ Previable PROM § Same as above § +pulmonary hypoplasia § +limb contractures • Before 20 weeks > baby needs fluid around it to develop lungs properly. If baby has ruptured membranes > then baby wont develop lungs. Wont survive. ***infections cause an inflammatory rxn in the cervix and uterus and the prostaglandin response is a/w uterine stimulation >>rupture of membranes releases prostaglandins OVER the cervix > stimulates dilation and effacement In majority of cases women will deliver w/in 7 days of ROM and this is almost always a/w pre-term birth

Uterine fibroids (leiomyoma or fibromyoma)

-benign tumor of uterus arising from smooth muscle cells of myometrium. Epi: 20% - 50% of women older than 30. Increases w/ age during reproductive years. -formation is estrogen driven and incidence increases during reproductive years until menopause. -formaiton and enlargemetn r halted post menopausally but do not completely disappear thus should tsill be considered as well. Atiology: Estrogen and progesterone equally promote uterine fibroid growth -abnormal vaginal bleeding is due to fibroid in the muscular layer protrude outwardly and becomes subserosal or submucosal fibroid (pedunculated) *Large uterine fibroids regardless of location can cause mass effects on bowel, bladder and cause urinary frequency, urgency and incontience as well as constipation. A. Submucosal fibroid: just below the mucosa inside the uterus > main cause of abnormal bleeding or dysmenorrhea (painful) B. Sub serosal fibroid: bulges out into the peritoneal cavity > compress bladder/bowel. C. Intramural: confined to myometrium. RFs: 1. Obesity 2. Age 40-44: 4th decade of life 3. Black ethnicity 4. Nulliparity: pregnancy is protective Hx: 1. RFs 2. MenorrHagia (Heavy periods) or bleeding between periods (spotting) 3. Irregular central pelvic mass 4. pelvic pain and pressure 5. Dysmenorrhea (D for Dard dara > painful periods due to cramps) 6. Bloating 7. Infertility 8. urinary complaints, constipation IX: pelviic pain 1. First pass urine > sign of infection 2. Beta HCG > rule out preg and ectopic 3. FBE: anemia > heavy bleeding 4. Pelvic Transvaginal ultrasound): most effective dx technique second only to hysteroscopy. 5. MRI 6. Endometrial biopsy 7. Hysteroscopy or laporoscopy Mx: only in sxmomatic pts Heavy bleeding: 1. Tranexamic acid: inhibits clot breakdown > slows bleeding 2. Mefanamic acid: control pain 3. The mini pill (progesterone only pill): no breaks thus some dont even get their periods. Thins endometrium and thickens mucus 4. GnRH analogues: suppress ovarian stimulation stopping fibroid growth. Bulk sxms: 1. Hysteroscopy resection of submucosal fibroid: risk of bleeding, damage, failure, infection, adhesions, anesthetic risk. 2. Uterine artery embolization: stop blood flow to the fibroid 3. Myomectomy by laparoscopy or by hysteroscopy 4. Hysterectomy: best when finished having kids. (Via vaginal or laparoscopic) Cxs: 1. Recurrent uterine fibroid growth: myomectomy is a/w reoccurence. 2. Labor and delivery cxs: breech, exessive bleed > PPH 3. Infertility 4. Acute torsion: causes pelvic and abdoo pain 5. Hemorrhage, aenmia: due to heavy bleeding. 6. Degenerative changes: presents during pregnancy w/ abdo pain and local tenderness at site. > red type degerenation: rapid growth that exceeds blood supply.

Secondary PPH

-bleeding after 24-6 weeks post partum -most common cause: A. Retained products of conception B. Post partum endometritisi: most commonly GBS, lactobacilli or exisiting STI C. Choriocarcinoma -bleeding is not as severe as Primary PPH but can still be fatal Ix: -high vaginal endocervical swab -regular BP checks -FBE, coags -Pelvic US looking for POC or an enlarge fundal height Mx: Prevention: -compression stockings -early mobility -clexane: post cesarean, or high BMI Mx: -retained POC: removal -infection: IV Abx -hysterectomy: last line option for persistent bleeding

Red cell isoimmune disease in pregnancy (Rhesus incompatibility)

-caused by destruction of fetal RBCs from transplacental passage of maternally derived IgG antibodies produced against RhD antigen. Freely crosses placenta > bind to RBCs and destroying them. More than 50 RBC antibodies potentially cause Rh incompatitbility. -Consequence is progressive fetal anemia, untreated > lead to hydrops fetalis (collection of fluid in serous compartments) and death. Epi: 15% of white poulation -Most common non-antiD antibodies are anti-K and anti-c. Aetiology: -caused by destruction of fetal RBCs from transplacental passage of maternal IgG antibody. -passage of fetal cells into maternal circulation -fetomaternal hemorrhage (amniocentesis/CVS, miscarriage, ectopic, GTD, APH) -placental trauma -ectopic pregnancy > lead to alloimmunisation and sensitization RFS -maternal Rh negative: only RhD + fetus from RhD postiive fathers sensitize their RHD neg moms to produce anti-D antibodies -feto-maternal hemorrhage: is common and detectable in 65% of preg. Only need .1ml of RhD positive fetal RBS to trigger immune resp. -invasive fetal procedures > amniocentesis and CVS -placental trauma -abortion: can sensitise RhD neg women -multiparity: primary maternal immune response to sensitisation by D antigen is weak, greatly enhanced when secondary immune resp is generated -omission of Rh immunoprophylaxis. -ectopic preg: alloimmunisation has occured where fetal RBCs r detactable in maternal circulation Hx: RFs *consequence of hemolysis > 1. ^ unconjugated bilirubin > can cause neurotoxicity known as kernicterus 2. Fetal anemia: -fetal hydrops (hydrops fetalis): hemolysis of RBCs causing hepatosplenomegaly and fetal ascites, ^ amniotic fliuld -death Pathophys: Exposure of RhD neg mom to RhD positive fetal RBCs > B lymphocytes >> IgG. -memory B lymphocytes await reappearance of RBCs in subsequent pregnancy. Second preg: these B cells > plasma cells >> IgG antibodies > cross placenta > attach on fetal. RBC > spleen > extravascular hemolysis >> fetal anemia. -fetus tries to compensate by ^ing EPO > this results in hepatosplenomegaly, portal HTN, cardiac compromise, tissue hypoxia, hypoviscosity, and ^ed brain perfusion. -Extreme fetal Hb deficits of 70 g/L or more can lead to hydrops fetalis (fluid collection) and intrauterine fetal death unless corected by intrauterine fetal transfusion or neonatal exchange transfusion following delivery Classif: -Rh D RBC alloimmunisation -hemolysis caused by RhD antigen -non RhD RBC alloimmunisation -Hemolysis caused by other ,atypical RBC antigens (Kell, RhC, Kidd, Duffy) IX; -maternal blood type: Rh- -maternal serum Rh antibody screen: + -fetal ultrasound: fluid in babies stomach is sign of severe fetal anemia -MCA Doppler: peak systolic velocity is ^ed in fetus w/ significant anemia. -Kleihauer Betke test: measure amount of fetal blood in maternal circulation -Rosette test: used to rule out significant fetomaternal hemorrhage -Cordocentesis (umbilical cord venepuncture): direct fetal hemoglobin assessment Management: RhD-negative mother -antiD immunoglobulin administered at 28 weeks and 34 weeks + following delivery (only in Rh + baby) -W/ massive hemorrhage or vaginal bleeding > Anti D immunoglobulin. -after amniocentesis or after CVS> Anti D given after any vaginal bleeding and after amniocentesis or CVS -fetus RhD positive and or severe fetalanemia > elevated middle cerebral artery flow or amniotic bilirubin levels > intravascular blood transfusions

Varicella Zoster:

-chicken pox during preg can be severe > VZV pneumonia -incubation is 10-21 days -risk if only w/ primary infection > in shingles the mother already has IgG antibodies thus the baby will have them and is protected. *IgG can only cross placenta 1st trimester infection > worse for baby 2nd and 3rd trimester infection > worse for mom Fetal cx: -vertical transmission is low 2% -can cause IUGR, limb hypoplasia, skin lesions, eye damage Mx: NIRS N I R: Mx: started to prevent maternal disease which can be severe -varicella immunoglobulins > must be w/in 4 days of exposure -aciclovir > w/in 24 hrs of infection and reduces severity of maternal disease S: screen household contacts

Gestational Diabetes complications

-maternal HTN: routine BP and urinary protein is needed. Pre-eclampsia is also ^ed in GDM and rx is related to ^ing glucose levels -cesarean section: due to macrosomia -fetal macrosomia: due to poor maternal glucose control. -neonatal hypoglycemia -neonatal polycythemia: bc baby is physically larger, it requries ^'er supply through placenta thus placental insufficiency may cause weak hypoxia > this stimulates EPO production in fetus > they are polycythemic upon delivery > this is the reason why the baby is red on delivery -neonatal jaundice: due to ^ RCC tuurnover in polycythemic babies -hypocalcemia -birth injuries: shoulder dystocia -neonatal death : still birth -insulin related hypoglyccemia: in insulin tx pts -recurrent gestational diabetes: recurs in 30-84% of subsequent pregnancieis -type 2 diabetes: most women w/ GDM eventually develop T2DM. Should be counselled about healthy lifestyle measures. -Risk of childhood obesity in these macrosomic babies is high

Incidental bleeding:

-more common origins of blood during pre and should be ruled out w/ speculum exam (once placenta previa is ruled out) Common origins include: 1. Cervical ectropion or cervical ectopy: glandular columnar epithelial cells from endocervix travels down to the outside of cervix. 2. Cervical dysplasia: cervical polyps or CIN > bleeding. Common in women who havent had pap smear. Ruled out on speculum exam after Us ruled out placenta previa. Mx after pregnancy to avoid cxs 3. idiopathic: 25% of Antepartum hemorrage r unexplained. Possibly due to migration of placenta or stretching of uterus. -CTG monitoring and maternal obs are important Hx: -trauma to the cervix? Can occur after sex, after examination -recent CST? Looking for HPV and cervical dysplasia.

Hyperemesis Gravidarum

-most severe form of nausea and vomitting in pregnancy (NVP) characterised by persistent vomitting, volume depletion, ketosis, electrolyte disturbances, and weight loss. -morning sickness begins between 4th and 7th week after last menstrual period. -Defined as: intractable vomitting a/w >5% weighht loss in pregnant weight, dehydration and electrolyte imbalance often requiring hospitalization Epi: Nausea and vomitting (early morning sickness) occurs in 75% of women Hyperemesis gravidarum occurs in 1 in 200. Aetiology: -high progesterone and estrogen levels -Due to high HCG levels -high progesterone decreases gastric motility > N/V Pathophys: -beta HCG > made by syncytiotrophoblast that invade into endometrial functionalis and allow placentation to occur. ***For the first 48 hours: BHCG doubles every 2 days, reaches a peak of ~50,000 RFs: -FHx of hyperemesis gravidarum -PHx of NVP -multiple gestation or increased placental mass -gestational trophoblastic disease -female fetus -Hx of motion sickness and miraines Hx: -rfs -first trimester nausea and vomitting: a/w Spike in HCG >starts at 4-7 week after last menstrual period and peaks at 10 weeks -weight loss >5% is consistent w/ hyperemesis gravidarum. -tachycardia -wernicke encephalopathy: visual disturbance, balance issues and confusion: excessive vomiting > thiamine def A. WerNICke triad: nic: nystagmus, imbalance, confusion -ketotic breath: suggestive of significant volume depletion due to hyperemesis gravidarum. A. Uncontrollable vomitting results in dehydration, weight loss, and ketosis. -features of dehydration: a. Headache, hypotention, postural dizziness, dry mouth, low urine output, ketotic breath a/w volume depletion Questions: -N/V -weight loss -headache, postural dizziness, dry mouth, fatigue Rule out: -twins > likely HG -GTD: vaginal bleeding. Pre-eclampsia sx: headache, visual disturb, swelling: occurs after 20 weeeks. -Gastro: sick contacts, food, diarrhea, fever, listeria (unpast dairy -appendicitis: migrating PU to RIF pain -UTI: storage FUND, flank pain, fevers. Ix: -urinalysis: ketonuria sign of dehydration -FBE -LFT -U&C: elevated -TSH and T4: low TSH in women with hyperemesis, elevated HCG. Decreased TSH, normal T4. -metabolic panel: : hypernatremia and hypochloremia. -Serum bHCG: risk of molar pregnancy -thiamine =pelvic ultrasound Mx: Nausea and vomitting -w/o volume depletion: dietary modification: eat smaller, more freq meals, avoid smells and food that cause nausea. Food should be bland tasting, high in carbs, low in fat. Sour (lemon) better tolerated than water. -ginger, acupressure: presssure is applied to P6: 3 finger widths above wrist > may be applied using wrist bands > treats nausea in pregnancy. 1st line: pyridoxine (B6) or doxylamine (antihistamine) 2nd line: metoclopramide (Dopamine antagonist antiemetics) or prochlorperazine (stemitil) suppositories if they cant hold fluid down. Hyperemesis gravidarum: W/ volume depletion: admit: -Iv hydration (ringer's lactate), glucose, thiamine (B1) to prevent wernickes encephalopathy. -anti-emetics: ondansetron IV or metoclopramide IM -PPI: omeprazole -corticosteroids (prednisolone) if failed other therapies

tubal Sterilization Females

-ovarian tubes r cut, sutured or cauterized to prevent passage of ovulated ovum into the uterus. -can be performed at time of cesarean -Women who want to becoem preg after may have microsurgical repair of fallopian tubes or may do in vitro fertilization (IVF). Complications: ectopic and miscarriage is higher .01% failure rate Benefit: 1. Performed at cesaren Cons: 1. Increase risk to women compared to male sterilization 2. Surgical risks

Implanon (progesterone only): 3 years arm implant

-placed in arm subdermally and secretes progesterone. -Prog > LH supression > thickens mucus and thins endometrium Replaced every 3 years Very small risk of failure Benefits: 1. Lasts 3 years 2. Removal allows quick fertility Better for younger women Cons: 1. Spotting or menorrhagia (heavy/prolonged periods) 2. Hormonal sensitivity: headache, N, depression, bloating 3. Hair skin changes CI: Liver disease Pregnant Breast cancer

Endometriosis

-presence of endometrial glands and stroma outside of the endometrial cavity and uterine muscle > affects intestines etc -Adenomyosis: presence of ectopic endometrial tissue within the myometrium > induces diffuse uteine enlargement. -Anteverted uterus: towards stomach -retroverted uterus > away from stomach. RFs: 1. Reproductive age 2. FHx 3. Nullparity 4. Mullerian anomalies 5. Late onset sexual intercourse: intact hymen closing vaginal outlet 6. Early menarche or late menopause Hx: Everything hurts so everything DYS: dysmenorrhea, dyspareunia, dysuria, dyschezia, decreased fertility 1. RFs 2. Dysmenorrhea: painful periods caused by cramps 3. Cyclic pelvic pain 3. Dyspareunia: pain during sex 4. Sub-fertility 5. Pelvic mass 6. Dysuria: if bladd or ureters r involved 7. Dyschezia (painful bowel movements) Epi: -7% of women -1 in 10 women -Most common dx in women presenting with pelvic pain and dysmenorrhea Aetiology: 1. Retrograde menstruation: endometrial tissue gains exposure to peritoneal surface 2. Deficient cell-mediated immune response: ineffective clearing of mensstrual effluent 3. Mullerian rests: occurs in pre-menarcheal girls > arise from mullerian rests > cells of paramesonephric origin stimulated by estrogen once maturation of HPA axis occurs. 4. Autoimmune disease 5. genetics Pathophys: -estrogen made in follicular phase promotes development of this glandular tissue (stratum functionalis) for implantation. Uterine artery > spiral artery enters into the endometrium and is Progesterone dependent. ^ LH > corpus luteum > progesterone. Low prog > vasoconstriction > slough off. -In preg: smooth muscle of myometrium increase Oxytocin receptors > ^ contractility. -Rectouterine pouch or pouchof douglas > most common locaion of endometriosis. -Distorted anatomy, and involvement of tube and or ovary due to scarring interferes with fertilization or implantation -Pelvic pain: dysmenorrhea occurs early stage of disease -Chronic pain is due to fibrosis that occurs with chronic inflammation > resulting in adhesions > distort normal anatomy. Ix: B-HCG test: pelvic pain and abnormal bleeding > miscarriage or ectopic must be ruled out. MSU: rule out urinary causes of pelvic pain FBE: for blood loss Iron studies rule out anemia Transvaginal ultrasound MRI Pelvis Hysterosalpingography in mullerian anomoly DIAGNOSTIC laparoscopy: direct viualization of implants at time of surgery and histopathology > enodmetrial glands or stroma outside uterus Endometriosis: A. Mulberry spots: dark blue/brown implants on uterine ligaments or within pouches B. Peritoneal burns:fibrotic lesions a/w endometrial tissue >mediate adhesion formation C. Endometrioma: AKA chocolate cysts: ectopic tisssue present on ovaries may bleed and form a cystic structure (dark and brown) D. Blebs: white nodules of earl disease -Surgery: increased risk of adhesions and need multiple procedures to fix recurring endometriosis. *women who gets hysterectomy bilateral salpingoophorectomy for endometriosis > will go to surgical menopause and requires estrogen but need to give a gap of a few months to let the ectopic endometrial tissue die then start on continuous HRT. Mx: Mini pill/mirena, implanon, depot provera (most become amenorrheic> thins endometrium and thickens mucus) or OCP: suppresses HPA axis thus supress Estrogen/progesterone secretion >atrophy of ectopic implants (endometrial tissue found in ectopic locations) NSAIDS Laparoscopy Fertility desired > clomifene, follitropin alpha (FSH), or IVF

Placenta Praevia PP (antepartum hemorrhage): non painful bleeding, non tender, no contractions

-presence of placental tissue overlying or proximate to the internal cervical os. Can be complete, partial, marginal or low lying. -Partial, marginal, low lying can resolve as preg progresses. -Complete PP wont move as preg progresses > will be central and low > in way of baby beign delivered vaginally -Cant do vaginal birth in PP. Must do cesarean section. -0.5% of pregnancies. Aetiology: -advanced maternal age -mutiple preg -smoking Pathophys: -blastocyts implants in lower uterine segment near cervical os. Presence of uterine scar in lower segment interferes w/ process of placentation >increasing risk of PP and abnormally adherent placenta (accreta on smooth muscle), increta (in smooth muscle), percreta (outer organs). -In PP > placenta is partly or completely covering cervical os > bleed may occur spontaneously from placental trauma (sexual intercourse or vaginal exam or as cervix opens at onset of labour. As the smooth muscle thins out near the cervix to accomodate growth of baby > placenta may be torn or separate (abrupt) from uterus > massive hamorrhage results. RFs -Previous Cesarean section: this puts a scar in uterus and the low lying placenta previa may also embed in the myometrium through the old scar known as placenta Accreta. -parity (births): multiple births -age -IVF: 2% risk of PP -PHX of PP -smoking Complications: -Major haemorrhage (bleeding) for the mother -Shock from loss of blood -Fetal distress from lack of oxygen -Premature labour or delivery -Emergency caesarean delivery -Hysterectomy, if the placenta fails to come away from the uterine lining -Death. Hx/Ex: -scarred uterus -rfs -painless vaginal bleeding >20 weeks gestation: ranges from light, mod, heavy, massive -Previous US anomaly in first trimester > may need MRI. -lack of uterine tenderness: most with PP bleeding will have non tender uterus -low BP and tachy > reduced blood ovlume secondary to hemorrhage. NO VAGINAL EXAM > risk of damaging placenta Main complicaiton > bleeding from spottin to severe hemorrhage. Grades rather than stages: Low grade: w/in 2 and a half cm to the os High grade: crosses the os. Ix: -Transvaginal US: identified at 20w > follow up at 34 w is required. Diagnosis: if placenta is found w/in 2.5cm of internal os at mid-trimester scan > follow up transvaginal scan at 34-36 to check site. -FBE > anemia -blood type and cross match: prepare for transfusion/surgery -INR/PTT, fibrinogen if DIC is present (petechia, ecchymosis, gangrene, mental disorientation, hypoxia, hypotension, GI bleed) -KB test: if mother is RH - : level of fetal RBCs determines the need for and amount of RH immunoglobulins. **Bleeding occurs outside the placenta. Mx: Admit if 3 bleeds have occured -Resuscitate mother > saline -Mom: DRS ABC > circulation is key. Plapate for uterine tenderness. Gentle speculum > NO Vaginal Exam! -Assess baby > CTG -Resuscitation: large bore IV, Blood for cross match, fluid, steroids -Bakri Ballon: instead of relying on smooth muscle to stop bleeding > insert bakri balloon. This is during and after cesarean: got baby out > pt is bleeding heavily > blow balloon before suturing the cesarean.

Pre-term labor

-preterm birth occurs btwn 24-37 weeks gestation. In 2/3 cases > spontaneous onset of labour -Threatened preterm labour: uterine contractions <37w w/o cervical change. Minority of women w/ preterm contractions (threatened premature labour TPTL) progress to actual labor and delivery. -the remainder of preterm birth is due to iatrogenic (for a maternal or fetal indication) delivery, most commonly bc of pre-eclampsia and IUGR. -PPROM: is rupture of membranes <37w gestation and prior to onset of labour. Epi: births before 37w > ~10% RFs and aetiology -previous Premature labour: 1 preterm > 4X rx, 2 preterm babies > 6.5X rx -previous cervical trauma (laser conisation, diathermy and LLETZ procedure) -maternal infections: UTI or Bacterial vaginosis (Gardnerella Vaginalis normal flora), or Systemic infections (listeria, malaria) -twin pregnancies: will deliver 3 weeks early on avg thus 1/2 of twin preg's r born preterm due to uterine stretch -short cervical length: <2cm -positive fetal fibronectin test -PPROM: 1/3 of preterm women, rupture occurs prior to onset of contractions. A/w a higher risk of maternal and fetal infection Weak RFS: IUGR, fetal stress, congenital abnormalities, smoking (strong dose relationsihp btwn smoking and premature labor), BMI <19 Iatrogenic causes: obesity due to oxidative stress >due to pre-eclampsia -drugs, smoking, OH, caffiene, psychological stress r all linked to early birth -polyhydramnios -domestic violence -poor dental hygiene Hx: -RFS -uterine contractions: uterine tightening is a normal physiological finding known as Braxton Hicks contractions AKA false labour. No dilation of cervix occurs. Contractions >1 in 10 inutes is less likely to be physiological braxton hicks contractions. -PPROM: membranes will rupture spontaneously in labour in most women. 1/3 > rupture occurs prior to contractions. ^ rx of infection -cervical dilation + regular uterine contractions >> labour is diagnosed. Closed cervix w/ uterine contraction is threatened premature labour. -cervical length <2 cm -^ed maternal/fetal HR: due to infection -lower abdominal or back pain -fever: systemic fever > malaria and listeria -vaginal bleeding: indicate antepartum hemorrhage due to placental abruption: a/w pain and uterine contractions.

Non hormonal: Copper IUD

-prevents fertilization from occuring as well as disrupts endometrium to restrict implantation -admin by clinic 99% effective Benefit: 1. Non hormonal with no hypersensitive effects Cons: 1. Heavier more painful periods 2. Risk of infection

Uterine rupture:

-rupture is one of the causes of PPH rather than antepartum hemorrhage but needs to be ruled out quickly Rupture of myometrium > damage to major uterine arteries > bleed into peritoneal cavity and vaginal cavity -bc of the high vascularity > there is high rx of fetal mortality and maternal morbidity. RFs -previous cesarean section: increase rx of cesarean scar rupture -cocaine use: a/w hyper stimulation of uterus > more liekly to rupture Hx: -peritonism -shoulder tip pain: blood in peritoneal cavity causes irritaiton of diaphragm -maternal collapse: hypovolemic and vagal shock -post partum hemorrhage: even after delivery bleeding continues. Ex: -peritonitis: rigid, painful abdomen on palpation -CTG: tachycardia or progressing distress bradycardia Mx: -Hemorrhage: IV access and fluids -Cesarean section: babies at severe risk when rupture occurs before delivery -hysterectomy: removed bc ongoing PPH can lead to maternal mortality

Gestational Trophoblastic Disease (GTD): pregnancy related tumors: rare, cells in womb start to proliferate uncontrolably.

-series of dysplastic conditions arising from cells of the implanting embryo -Hydatidiform moles: GTD is series of dysplastic conditions arising from syncytiotrophoblast (produces HCG) ****Grape like cysts on placental tissue Non cancerous: 1. Complete mole: no maternal chromosome: just dispermy (2 sperm) penetrating empty egg > 46 XX or XY complete mole. -Complete means total of 46. -No maternal chrom > thus no fetus -moderate rx of malignancy 15% due to ^ amount of abnormal tissue. -90% > invasive moles -10% > choriocarcinoma 2. Partial mole (triploid): Dispermy (2 sperm:46) penetrate egg w/ (23 maternal DNA/chromosomes) > 46 +23 => 69 XXX, XXY, XYY -to form a fetus: need maternal and paternal DNA thus may see fetus present in partial molar pregnancy -May even have a heart beat on US -Low rix of malignancy 3% Cancerous: PIC 1. Placental site tumors: tumor occuring many yrs after preg 2. Invasive hydatidiform moles: previously benign mole becomes malignant and moves to other sites> majority invades myometrium and myometrial vessels. ^'s rx of uterine rupture. 3. Choriocarcinoma: very aggressive tumor > occuring upto 15 yrs after last preg: -rare malignant neoplasm of trophoblastic cells > systemic mets (~30% of cases) to: A. Most common > vagina and lungs B. Less common > gut and brain. EPi: 1 in 1,000 pregnancies Aetiology: -not understood. -presence of excess paternal chromosomes. Pathophys: 1. complete hydatidiform moles: 46 XX/XY and entirely paternal DNA penetrating empty egg. 2. Partial hydatidiform: 69 chromosome: 2 paternal and 1 maternal DNA RFS: -age: extremes of maternal age: >35 and <19 -prior GTD: 10X rx of GTD -Blood group A,B, AB: a/w ^ed rx of GTD -smoking Hx: -rfs -present in 1st trimester preg w/ a hx of missed menstrual periods -missed period -vaginal bleeding: MOST COMMON SIGN 84%: light spotting to heavy bleeding and may include passage of hydropic vili -large uterus for gestational age: Partial molar preg may have smaller than anticipated uterine size due to fewer hydropic vili -Early onset pre-eclampsia: ^ BHCG play a role in onset of pre-eclmapsia > headache and photophobia: exacerbated sxms of pre-eclampsia -SOB and Resp distress: due to anemia -Hyperemesis gravidarum: early morning sickness N/V, dehydrated: sensitivity to BHCG. -tachy, tremor, insomnia, diarrhea -HTN: a/w complete molar preg -pallor: anemia -pelvic pain > theca lutin cysts: due to ^ BHCG which maintains corpus luteum and theca cells. -uterine bleeding -peripheral edema: anemia > lead to sxms and signs of high output cardiac failure. Cluster questions: -early preg bleeding, bleeding post D&C, N/V, dehydratiotn, pelvic pain Ix: -serum BHCG: abnormally elevated serum bHCG: >100,000 IU/L -FBE: anemia from persistent vaginal bleeding -Prolonged PT, PTT: greater rx of bleeding at time of evacuation w/ rx of DIC -LFT and GFR/UEC: need normal liver and kidney fxn for optimal dosing of chemo agents -TSH: cross-reactivity of bHCG and TSH may lead to thyrotoxicosis -blood group and hold w/ RH -pelvic ultrasound -CXR: canon ball lesion pulmonary nodules may represent metastatic disease. Pulmonary edema secondary to high output cardiac failure from anemia or hyperthyroidism. Alveolar infiltrates > sign of resp distress syndrome : see kerley B lines, alveolar infiltrates, interstitial markings, pulmonary nodules. -Placental tissue biopsy/histology DDX: -multiple fetuses (twins): larger than expected uterus and elevated serum BHCG -pelvic tumor: enlarged uterus and painless bleeding and adnexal mass. -spontaneous abortion: rx factors: older age, bacterial vaginosis, thrombophilias **Risk of future pregnancy w/ GTD is 1% or 10X the baseline risk) > followed closely in subsequent pregnancies. Mx: -admit, Iv fluids or blood transfusion, antiemetics for hyperemesis gravidarum or H2 antagonist, NBM, antihypertensives if required for Preeclamp >160/110 requires magnesium sulfate first line or labetaolol or hydralazine second line -Benign disease: dilitation and evacuation (same method of abortion/miscarriage) -Malignant disease: refer to oncology -Serial B HCG tracking: need to monitor b HCG post removal Contraception should be advised during the period of follow up (12 months) after evacuation of the mole) A. benign/complete mole > 6 months of follow up B. Invasive > 12 months of follow up

Surgical: Vasectomy sterilization

-small incision in scotum under local. Vas deferens is cut and sealed to prevent passage of sperm into the ejaculate -Ejaculate still exists > it just has no sperm -Risk of post procedure regret is highest amoung young men Admin in GP clinic if capable and a semen analysis should be performed 12 months later to ensure success 0.01% failure rate. Benfit: 1. Very effective 2. less risk than female sterilization thus should be pushed in preference Cons: 1. Risk of infection, bleeding, pain 2. Risk of anti-sperm antibodies develop affecting fertility after. (Worse chance reversal).

Placental abruption > really bad: painful, tender, contraction, bleeding

-total or partial detachment of placenta from endometrial decidual cells prior to delivery of fetus. -blood usually maternal leaks between placenta and the uterus -may be concealed -the placental interface is made up of fetal villus (blood vessels) supplied by umbilical arteries and drained by umbilical vein and maternal placental sinuses surround them. Ischemia > loss of attachment btwn endometrium and villus > detach Two types: abruption is revealed when: 1. Blood escapes through the vagina or 2. Bleeding occurs behind the placenta (concealed hemorrhage): women can lose a liter of blood internally before any vaginally bleeding > can lead to hypotension and shock, organ failure, DIC, PPH, fetal hypoxia RFs: -HTN -Pre-eclampsia -smoking -cocain use -PHx of abruption -trauma -chorioamnionitis -oligohydramnios (decreased amniotic fluid): strongly a/w abruption Hx: -can not have bleeding > concealed bleeding -painful -tender -contractions -fetal compromise > CTG -Maternal vitals > asses how bad it is. *abruption: painful, tender + contractions *in previa and marginal bleed: its painless and non tender and no contractions Ix: -Ultrasound -CTG for baby -FBE -Coagulation studies -Blood group and hold -KB test: in RH - mom Cxs: Mom: -acute blood loos -DIC -organ failure -PPH Fetal: hypoxia Mx: -Mom: DRS ABC, palpate for uterine tenderness/contractions, gentle speculum, large bore cannula + IV fluids -baby: CTG/KB test -Cesarean section when there is moderate (not severe bc thats when fetus is dead) abruption and fetal distress. Make sure mom is stabilized first -Dont forget anti-D in RH - mom -beware of concealed bleed Prevention of preterm cxs: -<34 weeks > betamethasone IM X2 +/- Tocolytics: suppresses premature labour long enough to give glucocorticoids to accelerate fetal lung maturity -erythromycin IV Cesarean sec

Rubella

-transmitted via respiratory droplets -vertical transmission is greatest in FIRST trimester as virus can cross placenta. Really important: <12 weeks: 90-100% rx of transmission w 90% rx of cxs >24 weeks: <1% rx of transmission with no rx of cxs Maternal infection fts: 1. Fine skin rash 2. Cervical chain lymphadenopathy 3. Joint pain and swelling: mainly wrists and fingers Dx: -presence of IgM antibodies to rubella antigen > these appear 1 week after exposure. -4x rise in IgG between initial and 2-3 week repeat > re-exposure *Vacination shouldnt be given until AFTER delivery bc its a live vaccine strain. Fetal cx: Since it mainly occurs in 1st trimester > causes developmental problems: developmental delays, IUGR, or death -Most common abnormalities include: CONGENITAL CATARACTS, SENSORY NEURAL DEAFNESS AND CARDIAC ABNORMALITIES (valvular stenosis) BUZZ Mx: NIRS: -notify and follow up as high risk -ID referal Reduce transmission: -1st trimester: TOP:termination of preg severe abnormality and ^ mortality -Screen household contacts IgG +, IgM + > possible recent infection or reinfection IgG-, IgM - > susceptible to infection IgG-, IgM + > possible recent infection IgG +, IgM - > previous infection or prior immunisation

Induction of labour

-undertaken when continuing a pregnancy is a/w greater level of maternal or fetal risk than delivery 4 reasons: 1. Gestational age: baby should reach term >37w in majority of cases 2. Indications for IOL: -hypertensive disorders: essential, gestational, or PET -diabetes: GDM -major medical conditions: renal, liver(cholestasis), heme (RH), neuro (eclampsia/seizures), thyroid (hyper/hypo) -placental insufficiency: IUGR or SGA -APH -fetal distress and hypoxia -twins: at 37-39 w -post dates: >42w 3. Contraindications to vaginal birth: -emergency delivery -placenta previa -^ rx cephalopelvic disproportion -multiple CS -active genital infection: herpes, NG, CT -twins w/ a breech twin 1. CI to oxytocics: -grand multiparity (5 previous deliveries): readily hyperstimulated -previous CS or uterine scar > careful to prevent rupture. -fetal distress -prematurity 4. Maternal preference: mom has right to decline medical intervention for labour and may want to allow nature to take course Hx: make sure baby was correct gestational age, meets the proper indication and has no CI for IOL and that it was her preferred option considering the risk. Ex: engaged fetus: If head is high and mobile > IOL is relatively CI due to small risk of cord prolapse w/ rupture of membranes > CS may be wise

Termination of preganncy

-vast majority of pregnancies r terminated before 20 weeks gestation (1st trimester termination) but may occur past this Epi: Abortion occurs in 1 in 4 pregnancieis 1 in 4 women throughout their life time Law: <24 weeks: medical prac may perform an abortion on a women. >24 weeks upto delivery: legal if 2 doctors agree that abortion is appropriate based on physical psychological and social circumstances Consent station IPBRAAD: Indication: what is it and why is it used Procedure: before, during and after Benefits Risks Alternatives Any questions Document and conset MGO PPDAFS Menstruation: LNMP: last day of period > add 7 days (day of ovulation) then add 9 months > this is expected delivery date. +/- 2 weeks and assums a 28 day regular cycle PGHx: -Sxms: burning, abnormal bleeding, ^ed urination, odor, d/c? -Gyne Dx's, surgeries -CST: date and result -contraception -POHx: GPA: number of preg, births, abortions/ectopics, miscarriages -Personal Hx: SADAM W: sleep, appetite, defecation, addiciton, micturition, weight -PMHx: illness/surgeries -Drugs: meds, herbs, recreational drugs, smoke, alcohol -Allergies -FHx: medical/gyne conditions, malignancies, cousins -Social: social support, marital status, occupation. Blood group: for prevention of rhesus antigen in RH neg mother. Examination: -vitals: hemo stable Ix: 1. Bedside B HCG test 2. High vaginal swab for infections (STIs) 3. Bloods: -Serum Beta HC: level: 1,500 is gestational sac, 10,000 > should see a heart -Blood group and antibodies : check for rhesus antigen and the need for anti D -FBE: if they r anemic 4. Ultrasound Mx: 1. Anti D: given to rhesus neg moms to prevent hematological problems 2. Prophylactic antibiotics: if infection 3. Discussion about contraception if there is time.

Antenatal Ix's

1. MSU: UTI 2. FBE: anemia: microcytic a/w Fe deficiency 3. Blood group and antibodies: important to avoid hemolytic disease of newborn. 4. Viral serology against: Hep B/C, HIV, Rubella, Syphilis, Varicella 5. Dating ultrasound: checks how many weeks preg u are and ur due date 6. CST: if not done within 5 years 7. OGTT: -fasting: greater or equal to 5.1 -1 hr greater or equal to 10 -2 hr: greater or equal to 8.5 Also in relevant pts: -HgB electrophoresis and Genetic studies: mainly in asian and mediteranean bacground pts for Beta Thalassesmia (electrophoresis) and alpha thalassesmia (H body staining or genetic studies) -serum ferritin (Fe storage): in vegeterian -vitmamin D: mainly in dark skinned (melaninin doesnt allow vitamin D to be made via sun) or covered women. -chalmydia screen: FPU PLUS Consider first trimester screening 1. NIPT 10w 2. Nuchal translucency scan: chromosomal abnormalities Trisomy 13,18, 21 3. PAPP A and B HCG levels

Menorrhagia (heavy bleeding Management)

1. Fe supplements and follow up 2. Hormonal A. Estrogen and progesterone: COCP: low Est > neg feedback on FSH> low FSH > decreased follicule development > low EST > cant thicken endometrium. Low Prog: inhibit ovulation and thin endometrium. B. Progesterone only (in women who are estrogen sensitive, older women, and ^'ed risk of DVT) > -Mirena (low dose PROG > thickens mucus to X sperm and thins endometrium. S/E: irregular menses for the first 6 months but lasts 5 yrs -Progesterone only oral contral contraceptive pill: Low dose thickens mucus and X sperm and thins endometrium. 3. Non hormonal: A. NSAIDS: mefenamic acid: reduce dilation of vessels of endometrium > decrease bleeding B. Tranexamic acid: ^ clot thus bleed less 4. Surgical A. Endometrial ablation > but decerase chance of pregnancy bc u ablate the stratuum basalis of endometrium thus ability to regenerate is lost B. Hysterectomy: after women has had family and is still bleeding. If almost about to reach menopause > then encourage to wait it out and wont need to do risky procedure

Abnormal uterine bleeding IX and Mx

1. First pass urine collection: STI screen 2. FBE: Fe def anemia 3. Fe studies 4. Coagulation studies 5. PCOS screen: OGTT, Testosterone, DHEAS, Lipids, Prolactin/progesterone 6. TFT 7. Pelvic ultrasound: -Polycystic ovaries: >12 2-9 mm cysts in the periphery of ovary or ^ ovarian volume. -Polyp inside endometrium -adenomyosis: BUZ thickening of transition zone with a venetian blind pattern of acoustic shadowing. -Leiomyoma > fibroid -malignancies > cervix/endometrium 8. Hysteroscopy dilation and curette 9. Cervical screening test 1. Tx the problem -remove polyps/fibroids > myomectomy -surgical tx of adenomyosis or malignancy -AB's for PID -Tx of thyroid and coagulapathy

CTG set up

Abnormal CTG > need more invasive ixs and may lead to emergency cesarian section External monitoring: place 2 transducers on abdomen of pregnant women -one records fetal HR and other records contractions of uterus. -limitations -to obtain acurate HR recordings during marked bradycardia, internal monitoring is needed Internal monitoring: scalp electrode + intrauterine pressure transducer IUP -intrauterine pressure catheter is used to measure uterine contractions and a scalp electrode attached to fetal head is used to monitor HR and more accurately w/ ECG trace -often combo can be used where fetal scalp electrode is placed w/o pressure catheter

Adult vs GD vs patient with diabetes

Adult: -Fasting: <5.5 (UL). >7 (L) -Random <5.5 (UL). >11 (L) Between you are uncertain: do OGTT DX: -fasting >7 -2hr post 75 g glucose >11 Diabetics: want to aim for: -Fasting: 6-8 -Post prandial: 6-10 HbA1C: 7% or less Waist circumferance: men <94cm and females <80cm GDM women: OGTT DX: -fasting >5 -1 hr >9.9 -2 hr >8.4 Aim for: Fasting: <5 2 hr post prandial <7

Later stage scans/ix's

1. 20 week morphology ultrasound: babys body and sex can be determined 2. 24-28w: OGTT: Fasting >5 1 hr >10 2 hr > 8.5 -FBE + group and antibodies 3. Week 28 and 34 > anti D injection 4. Week 36: right before term (37 weeks). -FBE -Group B streptococcus agalactiae swab (GBS swab): 1. Streptococcus: A. Alpha hemolytic: strep viridans, strep pneumonia B. Beta hemolytic: group A strep pyogenes, group B strep agalacticae. C. Gamma hemolytic: enteroccocus *GBS is normal flora of genital tract in 10-30% of women. During delivery, 70% of wome who have GBS will pass it onto baby. In 0.4% of cases > can cause mild pneumonia w/in first 7 days of life, neonatal meningitis *thus at 36 weeks (just before term) > vaginal and anal swab is taken for group B hemolytic strep + culture 36 week Intrapartum GBS antibiotics: benzylpenicilline 3g IV then 1.8g 4 hoursly until delivery. Clindamycin is alternative for MCQs. Pertussis vaccination: all women and partners r funded to get pertusis booster at 36/40 week, just before term. Recommend grandparents or care givers get booster as well (every 10 years).

Antenatal care: What to do: screens: 10, 11, 12, 15

1. Antenatal care: GP checks your overal health and gives advice on healthy habits > about 10 appointments -Antenatal tests include: 2. Weight and height: gain 10-15 kilos mostly after 20w and is due to baby growing and body preparing for production of milk 3. Dating Scan Ultrasound: ~12w (10-13w) to confirm due date. 4. Non invasive prenatal test (Cell free fetal DNA): ~12w (10w) > blood test : screens for chromosomal abnormalities Trisomy 13,18,21 but not covered by medicare or private health insurance. Costs ~$400. *REMEMBER this is just screening tool! 5. Nuchal translucency scan: ~12w (11-14): works out risks of chromosomal abnormalities: Trisomy 13 Platue, Edwards 18, Downs 21 -If at high risk: greater than 1 in 50 > refer to 6. Genetic counsellor to discus options for invasive Dx testing: 7. Chorionic Villus Sampling (^ Rx, >35 yo, or FHx): ~12 weeks (11-13w): Detects genetic disorders OR 8. Amniocentesis (^Rx, >35, FHx): done at 15-20 weeks. Draws 20 ml of amniotic fluid via US. Detects genetic disorders + NTDs -Detects chromosomal abnormalities, blood disorders, NTD's, MSK disorders 9. Morphology scan- ~20w (18-22w): detects babies body and placenta 10. Urine: albumin > signs of infection/pre-eclampsia 11. BP > preg induced HTN 12. Blood tests: A. Rheuss factor: checks for protein called D-antigen > give anti D injectioin to RH- moms @ 28 and 34 weeks of preg B. Iron C. Gestational diabetes: develop @ 24-28 weeks of preg D. Infections 13. CST: 25-74 yrs more sensitive at detecting the cause of cervical cancer > HPV 14. GBS test: swab taken at 35-37 weeks > give IV Benzyl Penicillin antibiotics. Allergies > Clindamycin

Dysmenorrhea (painful period) IX:

1. B HCG test 2. First pass urine > STI 3. FBE ESR/CRP 4. Pelvic ultrasound

Vulval mass

1. Bartholin's cyst and abscess -Bartholins duct cysts and gland abscesses r common in reproductive age. Gland lubricates vagina and r susceptible to infection -Bartholins gland AKA greater vestibular gland r at 8 and 4 o clock. RFs: reproductive age: 13-30 -After 30, get gradual involution of the glands. post menoapusal > will shrivel up => protective against bacteria getting in. Obstruction of duct > retention of secretions > cyst formation > may become infected with abscess in the gland. -Microbiology: > polymicrobial. A. Most common > Neisseria Gonorrhea B. Others: Chlamydia trachomatis, E. Coli, Staph aureus (MRSA) Hx: -cysts: often small and asymptomatic, non tender -larger cysts: dyspareunia, irritation, vulval asymmetry (distension of local tissue -Abscess: painful, red and swollen, irritatiotn, d/c, fever. Dx: clinical dx. -women >40 (unlikelly to have an abscess) > biopsy must e taken to rule out vulval cancer. Mx: Asymptomatic: -Sitz Bath: salt water bath Symptomatic: -word catheter: balloon inserted into cyst to allow continued drainage -marsupialization: longitudinal incision into cyst creating an open pouch. Daily sitz baths r req for 7-10 days + admission, analgesia, antibiotics. 2. Skene's Duct abscess: lubricates urethral meatus. Similar microbes above. Often asymptomatic. May cause urinary obstruction, incomplete emptying, dysuria when larger 3. Squamous inclusion cyst: MOST COMMON and occurs at site of episiotomy -result from trauma (laceration, episiotomy repair) that entraps viable epithelial tissue below the surface -fts : asymptomatic, white/yellow appearance. 4. Vulvar epidermal/epidermoid cyst: -due to occlusion of pilosebacious glands -occur over labia majora -classical sebaceous cyst appearance w/ central puncta. 5. Squamous cell dysplasia A. Vulval intra epithelial neoplasia a/w HPV 6 and 11 and cause condylomata (genital warts). Resolve spont. But 4% progress to malignant SCC. -Raised defined warts, itchy, sore, catch on underwear. Self resolve B. Vulval carcinoma: -predom SCC from HPV mediated VIN. -Raised lump or non healing itchy ulcer. Painless. 6. Lipoma: -benign tumors of adipose tissue mainly on labia majora. -Classical slipping sign. -large slow growing mass -Dyspareunia is main reason for excision. Others but not important.

Post partum hemorrhage Mx

1. Call for help: notify senior medical staff and midwife in charge: Anesetist and consultant when PPH >1,500 ml and ongoing 2. Resuscitate: -Airway breathing circulation -16 gauge cannula -venepuncture: samples for group and cross match, FBE, coagulation screen, including fibrinogen -high flow O2: 15L if major PPH -Rapid fluid volume replacement: crystalloid (Hartman's solution: sodium lactate) -IDC -keep women warm -vital signs every 15 minutes: if major PPH continue > pulse, BP, RR, oximetry 3. Explain what is happening to women and partner 4. Stop bleeding: A. Tone: -fundal massage > stimulate uterine contractions and remove clots Urotonics: 1st line > 2nd line >3rd > 4th line -Syntometrine 1ml IM: SEs: N/V/HTN: (Oxytocin with Ergometrine: ergometrine is contraindicated in women with hypertension, cardiac disease, asthma, severe PVD or placenta insitu) OR -Oxytocin 10 units when ergometrine is CI (asthma, HTN, cardiac disease: ergometrine causes HTN, while oxytocin causes hypotension). OR -Ergometrine 0.25 mg IM Second line: -oxytocin infusion 10 units/hr: Ae: hypotension, hyponatremia Third line: Misoprostol: 800-1000 micrograms per rectum or sublingual. -Ae: bronchospasm, HTN, N/V, takes 1 hour 4th line: carboprost IM -empty bladder > IDC -if still bleeding > Bakri balloon as first line surgical intervention, or B-lynch suture or haymans sutures or uterine artery embolization, or Internal iliac ligation, or radiological emoblizaitaon or hysterectomy. B. Tissue: -check if placenta and membranes r complete -if placenta is separated and retained > VE and remove RPOC -placenta not separated > repeat Oxytocin > transfer to theater for manual removal under anesthetic C. Trauma: -inspect perineum, vagina, cervix > apply pressure or suture to repair -surgery if cervical tear or uterine rupture D. Thrombin: -blood ix: clotting screen/disorder -antifibrinolytics: A. Tranexamic acid: CI w/ thromboembolic disease unless anti-coagulants given together). In women w/ renal impairement > reduce dose. 5. Blood: -give O negative blood, fresh frozen plasma, platelets, cryoprecipitate -start transfusion if women requires more than 4 unites of RBC and has ongoing bleedign

Cervical cancer ix's

1. Cervical screening test or high vaginal self sampling swab > if tested positive for HPV > 2. Liquid Based Cytology 3. If positive do colposcopy > stain with acetic acid and look at cervix: white lesions, Punctation: protruding lesions, abnormal BV's -cone biopsy: done to see how deep cancer cells have spread into tissue beneat surface of cervix. Wome presenting with intermentrual or post coital bleeding, dyspareunia or vaginal d/c need colposcopy straight away. CST: is just a screening test that screens for the cause of cervical cancer. The cause is detection of HPV DNA.

Women infertility Mx

1. Counsel them: I know its stressful but evidence has shown that stress interferes with treatment. Have UPSI for 1 year > there is an 85% chance of conception. UPSI for 2 years > 93% chance. 2. SAVES weight: stop smoking, alcohol, veggies, fruits, exercise, stress management, and weight loss 3. Draw cycle: Egg lasts 24 hours in the uterus, sperm lasts 72 hours in the uterus and tubes. Because its hard to pinpoint exactly when u ovulate, ideal one ovulates on day 14 but can occur anywhere between day 10-20. Thus its important to have sex on day 12, 14, and 16 every two days is adequate. After day 20, its highly unlikely to that the egg will be there. 4. Prepare for pregnancy: take folate 1-3 months before and continue upto 3 months after giving birth. Check rubella status: if not immune give it to them bc they cant get it if they become pregnant 5.Treatments: gonadotrophins or clomid to induce ovulation, IVF, surrogacy or adoption 1. Hypothalamic or hypopituitary anovulation (hypo-gonadotrophic) -Gonadotrophins: first line w/ hypothalamic amenorrhea. + -Human chorionic gonadotrophin hCG -counselling: it is highly stressful and there is evidence that stress is a/w treatment failure!!!! Second line: IVF + counselling 2. PCOS: (eugonadotrophic) A. Weight loss B. Counselling C. Metformin D. Controlled ovarian stimulation > Clomid E. IVF 3. Tubal > hypergonadotrophic A. IVF B. Counselling C. Tubal reconstruction 4. Endometriosis > hypergonadotrophic A. Clomid, counselling 2nd line: IVF 5. Age related > hypergonadotrophic A.counselling, + oocyte donation with donor IVF 6. Damaged or missing uterus Hypergonadotrophic: some form of ovarian failure causing no ovulaitaon) A. Surrogacy

Termination

1. Drugs: < 7 weeks -Mifepristone: causes placenta to separate from endometrium and causes contractions of uterus to remove POC (products of conception) + Misoprostol is taken w/in 48 hours orally or vaginally to cause contractions to remove all of the POC. 2. Surgical > must prime the cervix (dilate or soften the cervix by mechanical or medical (drugs) before procedure): >14 weeks - <14 weeks >> suction curettage - > 14 weeks >>Dilation and evacuation Between 7-14 weeks >> even distribution between drug and surgical Priming the cervix: done before surgical curettage to dilate the cervix and reduce force requrie to dilate the cervix > reduces risk of cervical damage, bleeding, infections. -Done medically by Misoprostol Perivaginally 200ug 3 hours prior: prostaglandin F2 Alpha dilates and soften cervix when locally given. A. 7-14 weeks > suction curettage -how: cervix dilated w/ metal dilators to allow suction currete and removing of POC. May or may not be sent for histology -when: <7 weeks > risk of failure is higher thus performed between 7-14 week mark. -very effective: risk of failure is 2/1,000 when performed after 7 weeks gestation. -Risks: very safe. Always talk about 5 cxs when u consent procedure: 1. Pain: may require oral analgesia 2. Bleeding: may continue for a week: report hospital if it gets heavier 3. Damage to local structures but rare. if damage occured > may need to do laporoscopy to fix it. 4. Infection: smelly, white discharge or f/r/n > report to ED 5. Failure: fail to remove all products but its rare 6. Anesthetic risk: may cause N/V . >14 weeks: Feticide + Dilation and evacuation: -Require Feticide: intra cardiac injection of potassium into the babies heart > then the fetus is passed intact or in clumps. -When: used in second trimester surgical terminations (>14 weeks) particularly those >20 weeks. -very effective -risks: pain, bleeding, daamge to local structures, infection, failure, anesthetic risk. Benefits: -day procedure -medical facility to mx any cxs -effective

Hypergonadotropic > Ovarian Failure.

1. Familial Early Menopause: Hot flushes? Vainal dryness? FHx of menopause? -genetic condition a/w early onset menopause and cessation of ovulation > thus no estrogen production. 2. Congenital: Any Primary amenorrhea? or Genetic diseases? (Only consider in primary infertility: never had a baby before). -Turners syndrome: absence of one X chromosome: physically > short, wide webbed neck, low set ears and hairline down the neck. Often amenorrheic and dont ovulate. -Fragile X syndrome: genetic condition >> intellectual disability, behavioral problems, and learning challeneges. Physical sxms: flat occicput, pointed ears. Most common single gene cause of autism and a/w infertility.

Germ cells (functional cysts)

1. Follicular cyst: -due to anovulatory cycles > the unruptured grafian follicle collects fluid in the antrum. Seen as simple fluid filled cyst on ultrasound. -sxmomatic when > rupture, hemorrhage or torsion. 2. Corpus Luteum Cyst: Fluid traps and forms a cyst. -resolves with menstrual phase of the cycle and no Beta HCG. -Sxmatic when: rupture or hemorrhage 3. Theca Lutin Cyst: sxomatic when rupture or hemorrhage -theca (major cell of follciular cyst) and lutin (major cell of corpus luteum cyst). -arise due to excess stim to atretic follicles via: A. Gestational trophoblastic disease: Beta HCG maintains role of corpus luteum and excessively high levels can stimulate the atretic follicles B. Ovulation inducing medication: -clomiphene citrate (estrogen antagonist) increases FSH production and stimulates ovulation. Non displastic causes of pelvic pain: 1. Ovarian torsion: mainly premenopauseal women with follciular or dermoid cyst on the ovary that causes it to tort Major red flag in pelvic pain > ruled out with doppler ultrasound of the arterial supply moving up into the ovary 2. Ectopic preg 3. PID 4. Appendicitis Tumors arise from primordial follicle in ovary. -In females majority r benign 97% but in males majority of germ cell tumors r malignant. Primordial germ cell tumors: 1. Poorly differentiated > dysgerminoma (rare malig tumor arising in young girls) 2. Well differentiated > A. Tissue similar to embrionic tissue > teratoma (dermoid cyst)> Rokitansky protuberance: most common ovarian tumor involving tissues from 3 germ layers: hair, teeth, sebaceous material B. Tissue similar to extra embryonic tissues > choriocarcinoma ( or yolk sac tumor (<30 yr old females > poor prognosis). Meig's syndrome: triad: benign ovarian tumor + ascites + pleural effusion

Antenatal exam:

1. General appearance: -are they fit and well? -fatiue and color? Anemia or thyroid issue 2. Height/weight, Vitals, urinalysis : BMI: weight in kg / height in meters then divide again by height in meters. Ex: 75kg / 1.65m /1.65m =26 kg/m2. A. <18.5 underweight B. >25 overweight C. >30 obese -Vitals BP <140/90 -Urine dipstick: Proteinuri: renal disease. Glycosuria: pre-existing diabetes 3. Heart: listen for valvular disease 4. Lungs: pulmonary edema a/w pre-eclampsia or poor cardiac compensation may be heard as inspiratory crackles. 5. Abdomen: General inspecation: A. Shape B. scars/stretch marks Fundal palpation: -fundus becomes palpable at 12 weeks. Palpate from xiphi sternum with edge of index finger until u hit the fundal pole -fundus height is taken from pubic symphisis to the fundal pole: number of cm= number of gestation (after 20 weeks) 1. 12-14 weeks: fundus just palpable above pubic bone 2. 20-22weeks: fundus palp > umbuilicus 3. Fundus drops at 40 weeks downwards as head descends into pelvis. Anterolateral abdo palpattion (feel sides) -fetal lie: lateral palpation assesses main body of uterus to confirm lie and identify fetal position. -fetal back > firmer *one hand gently placed on one side of uterus to apply pressure > other hand > finger tips to identify what is found (performed on both sides). -difficult lateral palpation > may indicate post. Position of baby Deep pelvic palpation: Fetal presentation and engagement: -identify which part of fetus will pass through pelvic brim first: normally the head -warn pt that it may be uncomfortable bc deep palpation is required -width of 5 fingers is guide to the expression in fifths of the head above the brim. -as head descends, portion of the head remaining above the brim, will be represetned by fewer finers: 4/5ths or 3/5ths *Head is engaged when the portion above the brim is represetned by 2 fingers width or less. *Is head engaged? Head is engaged when head accomodates 2 fingers above the brim Auscultation: -fetal heart rate: 110-160bpm. Take moms pulse to ensure this is not being auscultated. -record and date first fetal movement called quickening > feeling of having flutters or gas A. Primigravida: 17-20 weeks B. Multigravidad: 16-18 weeks Legs: peripheral edema: signs of pre-eclampsia or normal cxn of pregnancy Summarise: -name, age, GPA, weeks gestation according to palpation, fetal lie, fetal presentation, fetal HR.

Cervical cancer HPV questions

1. Have u had the HPV vaccine? 2. R u sexually active? Is it unprotected? At what age did u start having sex? 3. Intermenstrual spotting or post coital bleeding?

Polycystic Ovarian syndrome Omg test DHEAS LIPS ProPerly

1. Hyperandrogenism 2. Oligo or anovulation 3. Polycystic ovarian morphology on ultrasound RFs: 1. FHX of PCOS 2. Early adrenarche (early onset pubic/axillary hair): PCOS develop in 50% of cases 3. Obesity 4. high levels of BPA (bisphenol A) is observed in PCOS women. Aetiology: Defects in HPA hypothalamic-pituitary axis: leading to androgen over production due to 1. Increased amplitude pulse of LH 2. Defects involving the ovaries 3. Inherited Pathophys: 1. Obesity/sedentary lifestyle > Increased GnRH pulsatile Release > increased LH: FSH ratio: ^ LH > theca cells > androgen excess 2. Obesity/sedentary lifestyle > insulin (inhibited by metformin) resistance (T2DM/dyslipidemia/heart disease)> hyperinsulinemia > androgen excess 3. Androgen excess (inhibited by OCPs) causes hirsutism, acne, alopecia. 4. Excess androgen > arrest secondary follicle (antral follcile) development >> A. Anovulation (inhibited by clomiphene citrate, metformin) > anovulatory bleed (irregular cycles) and subfertility (impaired oocyte development, high rate of miscarriage and obstetrical complications) B. Annovulation > (no corpus luteum) > decreased progesterone release > get unopposed increase in estrogen > breakthrough bleed > unopposed estrogen causes endometrial hyperplasia > increase risk of endometrial cancer. Increasing insulin decreases production of sex hormone binding globulin > low SHBG > more unbound androgens in circulation. *Estrogen breakthrough bleeding occurs when excess estrogen stimulates endometrium to proliferate (hyperplasia) > will get heavy bleeding which can be mistaken for a real period. With insufficient progesterone > portions of endometrial lining slough at irregular intervals. The normal progesterone vasoconstriction and platelet plugging dont take place resulting in profuse bleeding. EPI: 8% of women or 1 in 5 women Hx: 1. RFs 2. Female reproductive age 3. Irregular menstruation: oligo or anovulation > menses at intervals less than 21 or >35 days (irregular cycle) 4. Infertility 5. Hirsuitism 6. Acne 7. Over weight and insulin insensitivity 8. Scalp hair loss 9. Oily skin, excess sweating, acanthosis nigricans Ix: Omg Taste DHEAS Lips Properly 1. BHCG test: everyone is pregnant unless proven otherwise. Women complaining of amenorrhea -OGTT, Low sexhormone binding globulin SHBG due to inhibition of liver by hyperinsulinemia 2. Serum Testosterone 3. DHEAS 4. Lipids 5. Serum: LH:FSH >3, prolactin and progesterone (done on day 21 luteal phase) 6. TFTs: TSH levels > thyroid dysfucntion presents with oligo or anovulation or menometorrhagia 7. pelvic ultrasound: string of pearls on ultrasound: -US done in early follicular phase after period - > 12 or more follicles in each ovary measuring 2-9 mm in diameter and or increased ovarian volume (>10 ml) in one or both ovaries. Endometrial lining >5-7 mm in thickness indicates endometrial thickening in the follicular phase) Mx: 1. Saves Weight: stop smoking, alcohol, vegies/fruit, exercise, weight loss: weight loss of 5-7% restores ovulation by reducing hyperinsulinemia and thus hyperandrogenism. 2. Metformin: if weight loss is unsuccsessful > metform is added > restore ovulation/menses to point where conception is possible but need to take it for 6-9 months. Increases ovulation and pregnancy rates. -continuing metforming through pregnancy may decrease rates of early pregnancy loss and premature birth 2.5 OCP > control menstrual irregularity and excess androgens > estrogen made by ovaries VIA FSH and LH >progesterione. Small exoenous estrogen and progesterone inhibits FSH and LH production thus no excess androgen production. Yasmine increases risk for DVT 3. Clomifene: anti-estrogen > inhibits estrogen negative feedback on hypothalamus >> increases FSH that may allow follicular maturation and ovulation. -5-10% risk of multiple pregnancy. Clomifene only > multiple pregnancy in 6%. Clomifene + metformin >3.1% -If 3 treatments of clomifene have failed > add metformin > converts clomifene resistent pt to a sensitive one. 4. Second line: follitropin alfa (FSH): high risk of multiple pregnancies: 20-30% twins, 2% triplets. 5. Laser hair removal and adapalene for acne

Infertility DDX

1. Hypothalamic: diet, exercise, stress, BMI 2. Pituitary: prolactinoma/adenoma, Sheehans syndrome (secondary) 3. Ovarian: -simple anovulation -PCOS -Premature ovarian failure -congenital syndromes 4. Uterine: -Polyp or Fibroid -Synechiae -PID -Perforated appendix -Endometriosis 5. Systemic: -Hyper/Hypothyroidism -Cushings

Primary amenorrhea and delayed puberty:

1. Hypothalamic: diet, exercise, stress, low/high bmi. Kallman's syndrome 2. Pituitary > prolactinoma/adenoma 3. Ovarian: turners syndrome, PCOS 4. Uterine: imperforate hyman, mullerian agenesis, androgen insensitivity, inter-vaginal septum. 5. Systemic: constitutional delay, hyper/hypothyroid Undifferentiated gonad fetus: Male: has sex determining region on y chromosome SRY gene: 1. Testes have leydig and sertoli cells: -sertoli cells > anti-mullerian hormone (AMH) > inhibits uterus and fallopian tubes. -leydig cells > testosterone > produce penis and seminal vesicles. 2. Female: has no SRY gene > produce ovaries and vagina. Infancy: -Male babies have high LH > leydig cells > produce testosterone from adrenal cortex > desend testicles -female babies have increased levels of FSH and estrodiol to stimulate oocytes to begin meiosis and arrest at Metaphase 2. -females get period by 12 but develop sexual characteristics by 10, males get sex charac by 12. Puberty in females: 8 -> 13. 14 years is delayed: Breast looks like 8. Thus add 5 = 13. Thus puberty is from 8-13. But 14 is delayed. Period: get it between 10-15 years old. 16 years old is delayed. Period: 10-15. Vagina is a hole thus 10 > add 5 = 15. Delayed is 16. DDX: 1. Hypogonadotrophic > hypothalamus/pit A. Diet, stress, heavy exercise > menarchy affected. B. Kallmans syndrome where no GnRH is produced (congenital) > main ft > Q's: lack or reduction in sense of smell? C. Prolactinoma/adenoma: Q's: morning headdache? 2. Imperforate hymen: canal is sealed by hymen w/in labia minora. Affects menarache => Q's: cyclical pain, suprapubic pressure? 3. Structural abnormalities: Septated uterus => cyclical pain? 4. Mullerian Agenesis: AKA uterovaginal agenesis. mullerian agenesis is caused by failure of mullerian duct thus get agenesis or underdevelopment of vagina, uterus or both. Vaginal canal is shortened. Ovaries r normal. -25% of cases there is renal anomoly causing ^ BP. Q's: No defined vagina? Elevated BP? 5. Androgen insensitivity: -child is XY genetically > develops testis but bc peripheral tissues r insensitive to testosterone > does not chagne from vagina to penis thus baby has a vagina. Uterus formation is inhibited by AMH from sertoli cells. The excess testosterone gets converted to esterone peripherally causing female characteristics (breasts) -have small/normal vagina but NO uterus. -Differentiated from mullerian agenesis by karyotyping (XX vs XY) as well as high levels of serum Test. Androgen insensitivity: the gonads are testis producing high testosterone. Have a vagina but no cervix. Q's: breast development with no secondary hair? Small vagina Hypergonadotrophic > ovarian failure: 1. Turners syndrome: high FSH/LH. -absence of second X chromosome thus only 1 X > so its only in females. -short stature, small ears, neck webbing, delayed puberty/mecnarche. Otitis media recurring, coaractation of aorta, normal intellectual profile. Q'S: recurring ear infection? Eugonadotrophic: PCOS: LH is going to be high and FSH is going to be low. -androgen excess a/w PCOS leads to hirsutism. -Rapid GnRH pulses > pituitary > HIGH LH over FSH, insulin insensitivity thus hyperinsulinemia. Others; 1. Constituional familial: late onset puberaty and menarche 2. Thyroid: hyper/hypothyroidism. Heat/cold intolerance?

Cardiotocography CTG

1. Hypoxemia: decreased arterial O2 concentration: but adequate Tissue and organ O2: can last for days to weeks. -chemoreceptors in arterial circulation initiate a compensatory response to reduce O2 consumption >> -Reduced fetal movements >>one of the reasons we ask this question -reduced growth: longer term 2. Hypoxia: decreased availability of O2: decreased arterial O2, decreased tissue O2, adequate major organ O2: last Hours -peripheral tissue ischemia is a big indicator that major organs and death will occur soon thus we see: A. Surge of stress hormones: NA and Cortisol > mediates peripheral vasoconstriction and ^ contractility of myocardium >> ^ HR B. Redistribution of blood flow: to major organs resulting in peripheral ischemia > anerobic respiration in cells. -peripheral tissues r very resistant to reduced O2 supply and as long as there is adequate central perfusion > there is no damage to fetus. 3. Asphyxia: deprived of oxygen: lasting only minutes or else result in organ damage and death -Decreased Blood, tissue, major organ O2 >> get: A. Max SNS and stress hormone response to ^ HR B. Glycogen stores from muslce and liver must be used to protect the brain which relies on free glucose in the blood. —> the brain and heart fail first. -normal baby will increase HR w/ contractions of uterus (bc uterine blood flow is constricted) > tells us about Heart and nervous system (has to be able to increase HR) >>thus gives idea about fetal well beign

Investigations for infertility in males: MSA AA:

1. Male Semen Analysis + Antisperm antibodies -Sperm analysis collection: No ejaculation for atleast 2 days. Need 2 tests, 6 weeks apart. Donated at center or at home w/ special catch condom. -Sperm antibodies r also tested and develop after vasectomy . Causes of infertility in men: A. Formation: Dx by hormone studies: FSH, LH, and testosterone 1. Congenital: kallman's syndrome, klienfelters (47XXy), androgen insensitivity (XX male) 2. Endocrine disturbances 3. scrotal temperature (undescended testis, varicocele) 4. Sperm autoantibodies post vasectomy or post undescended testis or other immune conditions. 5. Systemic disease: viral infection, chronic disease B. Transportation: Dx by ultrasound of the vas and prostate 6. Congenital anomoly 7. Urogenital tract infections: Hx of STIs 8. Cystic fibrosis 9. Malignancies C. Ejaculatiotn > Erectile dysfunction or ejac problems. D. Idiopathic > 30% of cases. Terminology: 1. Azospermia: spermatozoa absent 2. Oliozospermia: spermatozoa are low <15 million/ml 3. Asthenozospermia: <32% progressive motile spermatozoa 4. Teratozospermia: <4% normal. Terato > looks like teratogen > abnormal morphology OAT: oligo-asteno-teratozospermia syndrome: WBC's in the ejactulate can be a sign of infection Semen pH should be more alkaline >7.2. More acidic semen > may have a blockage in the flow of semen. sperm antibodies r also taken.

Contraceptives

1. Nothing: abstinence 2. Medical: A. Hormonal: -estrogen and progesterone > COCP -Progesterone only pill: mini pill, Depot, Implanon (3), Mirena (5) B. Non hormonal: barriers, copper IUD 3. Surgical: -vasectomy -tubal sterilization 4. Natural planning: -rhythm/calendar -billings cervical mucus method -symptothermal

All gyne histories need: 6 P's

1. Periods: -first/last period -length, heaviness, history of complications, pain, regularity. 2. Pain: regular pain during periods, sex or other? 3. Pus: d/c, Hx of STI's and last STI check 4. Pee: urinary symptoms or Hx of UTI's 5. Pausal: menopausal sxms 6. Penis activity: r u sexually active, regular partner? Pain or problems during sex?

All antenatal counseling stations need:

1. Planned or Spontaneous (IVF) preganncy? 2. Folate: 3 months before, 3 months after knowing ur pregnant 3. Check rubella and varicella serology (ones you cant give during pregnancy. 4. During pregnancy: make sure you get the influenza and whooping cough vaccine 5. Regular review

Natural planning

1. Rhythm/calendar: -can use this if ur cycle is super regular -can work out that 14 days before your regular period is when u ovulate so u abstain for the week before and after this. Failure rate is high Benefit: 1. No contraception needed Cons: 1. Risky and need regular periods 2. Still need barrier method 2. Billings method: -timing intercourse for fertility but ppl also think it can replace contraception -normally the mucus can be thick and stretchy -when u r ovulatin the mucus goes thin, clear and increased in volume -Ovulation: thin, high volume, clear. -High failure rate.

Prevention of preterm labour: talk about this risk factors

1. SAVES W: Stop smoking/OH, Veggies/fruits, exercise, stress control, weight loss: 80cm for women, 94cm for men. 2. Treat bacteuria/urogenital infections pre pregnancy: an MSU is a common test in antenatal period 3. Consider need for cervical suture: prevents dilating before there is ripening thus mainly in threatened PTL (contractions w/o dilation) 4. Vaginal progesterone: promotes myometrial quiescence thus vaginal administration helps reduce delay labour.

Eugonadotropic > Ovarian Dysfunction

1. Simple Anovulation: Any menstrual irregularity or heavy periods? -Simple anovulation: normal follicular development but no ovulation (thus no progesterone) 2. PCOS: Facial, pubic, axillary hair? Acne, oily skin, allopecia, weight gain, irregular menses? -Get insulin resistence (thus high insulin levels), plus Low FSH and high LH. -Low FSH > prevents maturation of follicle in ovary thus get anovulation (infertility)

Post partum management

1. Skin to skin contact: helps with thermal stability of mom and increases oxytocin release to promote let down of colostrum 2. Maternal obs: first hour > every 15 mins. Then 3 hourly. -Oxytocic drugs: stimulates contraction of uterine smooth muscle and dilation of vasculature >> can get HYPOTENSION 3. Analgesia: oral paracetamol, PR Diclofenac (voltaren) is used following perineal sutures, cold packs to reduce swelling 4. Baby weight: normal weight 2.5-4 kg 5. Prevention of cxs: A. Thromboembolism: early mobility, compressive stockings, clexane (used post LUSCS-due to spinal anesthetic) or w/ BMI >30 B. Infections: review of surgical sites C. Urinary retention: IDC following spinal or epidural D. Constipation and hemorrhoids: diet w/ ^ fiber + fluids E. Incontinence: physio F. Low mood and post natal depression: basic mx: early or additional domiciliary visits, social work/psychologist review. -More significant depression and psychosis: do psych review 6. Mother education: A. Lochia: progressive dischage changes from red > pinkish brown > yellow-white over 2 weeks B. Amenorrhea: can last upto 6-8 weeks or longer if breast feeding C. Fertility: contraception should be used: can do implanon, or condoms but no COCP if breast feeding D. Breast changes and breast feeding > refer to lactation consult E. Baby: sleep on back with head uncovered with minimal toys in cot F. Maternal sleep, nutrition and exercise is good G. Motor vehicle restrains 7. Anti D: all RH negative women will receieve anti- D injection at 28 and 34 weeks. An additional dose of Anti D is given to RH- moms who deliver an RH + baby. Baseline dose > 225 international units. -if theres maternal exposure (PPH or placental abnormaliities) > a Kleihauer test is used to determine dose. 8. Vaccination: -can get MMR or varicella now bc u cant get it during antenatal period. Should be given while in hospital Discharge: -NVD > 1-2 days -CS> 3-4 days HOME: Week 1: domicillary follow up: midwife comes to follow up within first 3-4 days post partum. Week 2-6 maternal child health nurse: follow up with mom and baby for initial 6 weeks Week 6: GP follow up: if mom has GDM > do a OGTT 6 weeks later to rule out persisting insulin resistance. -pre-eclampsia > BP, urine PCR

Preterm labour Mx: STATIN

1. Threatened premature labour (contractions <37w w/o cervix change) -assess mom: do fibronectin test: helps identify women who r likely to deliver shortly (high risk) -fetal monitoring: CTG -method of delivery should be considered > Cesarean section 2. Preterm Premature Rupture of Membranes PPROM: -mom: monitor for signs of infection: tachy, pyrexia, uterine tenderness, offensive vaginal d/c, ^WCC/CRP -fetal HR CTG >160 tachycardia > sign of chorioamnionitis. -Antibiotics: Erythromycin or phenoxymethylpenicillin. Dont give amoxicillin/clavulanate > ^ rx of NEC in neonate. -Corticosteroid if at 24-34w: dexamethasone PPROM > 34 weeks or Chorioamnionitis: Consider induced delivery from 34 weeks if there r comorbities present (oligohydramnios, abnormal doppler, pre-eclampsia, chronic HTN. -chorioamnionitits can cause neurological damage in fetus. Once found > delivery is indicated ASAP. 3. High risk of imminent delivery without PPROM A. maternal and fetal assessment: -high risk of imminent delivery at 24-34w gestation is evidenced by regular uterine contractions, cervical dilation, or positive fetal fibronectin test. B. Corticosteroid: dexamethasone 6mg IM: all women at rx of preterm delivery w/in 7 days who r from 24-34w should get dexamethasone > lowers rate of intraventricular hemorrhage. -If given later in preterm: 35-36w > may reduce neonatal respiratory cxs AEs: multiple doses r linked to IUGR and long term morbidity. C. IV Benpen or clindamycin: *all women in active premature labor w/ uterine contractions and cervical dilation r given antibiotics for GBS prophylaxis. D. Tocolytic (uterine contraction ceasing): prolongs gestation btwn 2-7 days > gives time to give corticosteroid. -Tocolytic > Nifedipine (Calcium channel blocker) SUMMARIZED MX for preterm labour: Preterm mx: STATIN Mx of preterm labour: S: Steroids dexamethasone when <34 weeks. Helps with lung maturation, GIT shincter formation, renal maturation, HbFetal to HgB adult 2X doses of betamethasone (celestone) 11.4mg IM 24 hrs apart. T: Transfer to tertiary center that can manage preterm infant A: Antibiotics: -Erythromycin and ampicillin is given in moms dx with Preterm premature rupture of membrane (PPROM: water broke <37w. ): reduces maternal and neonatal morbidity, delays delivery allowing sufficient time for prophylactic CCS. Amoxicillin/clavulanate ^'s rx of neonatal Necrotising enterocolitis. -IV Benpen or clindamycin in all women in active premature labour w/ contractions and cervical dilation for GBS prophylaxis. *****chorioamnionitis: AMG: ampicillin, metronidazole, gentamycin T: Tocolytics (uterine contraction ceasing: Prolonges estation btwn 2-7 days > gives time for CCS to work A. Calcium Channel Blockers: Nifedipine: Contraindications: >34 weeks (closer to term), maternal cxs (PPROM, APH, placental abruption, infection, fetal distress) I: Intrapartum Care: pediatric and obstetric presence at delivery with fetal and maternal monitoring. Can be vaginal/CS: any abnormal maternal/fetal signs >> CS bc instrumental delivery on premature fetus can have consequences N: Neuroprotection: <30weeks: -maternal IV Magnesium Sulfate infusion: provides neuroprotection of fetus and decrease rx of death and disability a/w cerebral palsy

Bowel and bladder

1. Urinary retention: -perineal pain > analgesia and IDC may be needed -pelvic floor dysfunction > physio 2. Bowel pathology: -constipation > due to opiate (pethidine), abdo pain low mobility -hemorrhoids > a/w ^ straining > surg review -fecal incontinence: grade 3 or 4 tears may cause fecal incontinence and require ongoing physio consultation Mx: Urinary retention: IDC and analgesia until mobilization and can pee Bowel: -prevent constipation and reduce aggrevation of hemorrhoids >> ^ fiber, water exercise, stool softener (lactulose) -severe urinary/fecal incontinence > refer to specialist

Secondary amenorrhea Ix's

1. Urine and serum B-HCG 2. Gonadotrophic hormones: estrogen and FSH + progesterone and LH -FSH on day 3, LH mid luteal day 21 with progesterone (corpus luteum) 3. Serum prolactin: for prolactinemia 4. TSH 5. Pelvic ultrasound Hypogonadotrophic: think central in hypothalamus/pituitary: -diet, exercise, stress. -pituitary failure > infarction, pituitary tumor Eugonadotrophic: PCOS -Ix: ^ total and free testosterone, DHEA (dehydroxyepiandrosterone), and 17 hydroxy progesterone, serum prolactin, OGTT, fasting lipid Hyper > ovarian failure: 1. Premature ovarian failure (menopause) 2. Congential abnormalities > think karyotyping for turners

Decreased maternal supply

1. ^ stimulation: greater the stimulation > greater the drive for breast milk >> ^ frequency of feeds and expressing 2. Review by lactation consultant : maximize psoition of mom and baby 3. Pharmacotherapy: Domperidone: -dopaminergic antagonist: if you block dopamine > remove prolactin inhibitory hormone > ^ Prolactin > ^ milk production *Secretion of prolactin is under the control of Dopamine (Prolactin inhibitory hormone) Breast engorgement: -on day 4 post partum: full, tight, and sore when attempting to breast feed -express milk before baby tries to suck Coughing or vomitting during breast feedign: -often when babies r really young they can tolerate fast flowing milk from breast -reassure its normal and feed against gravity is important Milk stasis: -when there is ^ period btwn expression, milk can be obstructed in the ducts -hot and cold packs or massage before/after feeds or in teh shower can promote milk flow. Mastitits: Pathophys: -infection and associiated inflammation of portion of lactiferous tree -arises when there is poor emptying of breast, nipple damage, blocked milk ducts, or tight bra > causes obstruction Cause: -staph aureaus > from skin which makes its way into the system HOPC -FRN, tender, swollen quadrant Tx of mastitis: -outside strep, stap >> methyl penicillin flucoxacillin -breast feeding is fine during mastitits and when on ABs -cool packs post feeding can reduce discomfot Prevention: -regular feeds 8-12 times a day -if baby is sleeping and breasts r full and sore > wake them up for a feed. -offer both breasts each feed. If finishes on one breast > alternate to other breast next feed. -express milk -avoid pressure on breasts (tight bra's) Cxs: -breast absecess > require surgical/US drainage -localized collection w/in breast Nipple Discomfort and errosions: -a degree of this is normal when starting bc nipples r more sensitive and baby is getting used to feeding -good nipple attachment prevents nipple trauma but when cracking/bleeding ocurs > hygiene is important to prevent mastitis such as regular changing breast pads, clean nipples in shower Mx: -express for a few days and nipple shield can allow nipple to recover

Primary amenorrhea ix's

1. beta HCG to rule out preg 2. FSH and LH, Prolactin for hyperprolactinuria (inhibits FSH/LH) 3. TSH: hyper/hypo 4. PCOS screen: OMG taste DHEAS Lips properly: -OGTT, testosterone, DHEAS, Lipids. Progesterone and prolactin levels -Low SHBG and mildly high Test is a/w PCOS -Normal SHBG and high androgens a/w androgen insensitivity - differentiate from pcos on ultrasound 3. Karyotyping: androgen insensitiivty XY female, looking for Turners (High FSH and LH) 4. Pelvic ultrasound

Cephalic Presentations

4 variations of cephalic presentation: 1. Vertex: normal: full flexsion, suboccipitobregmatic (SOB):9.5cm, 2. Deflexed vertex: slightly deflexed, occipitofrontal 11.5cm. 3. Brow: moderately deflexed, occipitomental 13.5. 4. Face: deflexed, submentobregmatic 9.5cm Bottom 3 > baby must be in occipitoposterior OP position. -for deflexed presentations to occur > need to be in an OP position *OA position (face towards ass) allows flexed vertex and suboccipitobregmatic diamter to present 9.5cm *Deflexed vertex: occipitofrontal 11.5cm > need to be in OP position. W/ an OP there is deflexion of babys head and so there is a larger diameter to stretch the vaginal entrance Dx: -abdo exam > anterior fetal limbs > suggests OP position > rx of obstruction is very high but not impossible -VE > palpable OP Management of deflexed vertex posision: 1st staage: -make sure labour is progressing normally: primi: 1cm/hr, multi 1.5cm/hr -continuous CTG monitoring -regular maternal obs -analgesia 2nd stage: intervention > rotational forceps: -commonly do a manual or instrumental rotation > can be rotated using vacuum or the keillands forceps -other outcome > do a cesarean. Brow presentation: 13.5cm: most unfavorable: looking up position -generally prevents vaginal birth -low incidence <1 in 500 live births -OP position VE: palpable OP + orbital ridges: feel anterior diamond fontanell as opposed to triangular posterior one. Mx of brow presentation: 1st and second stage: Cesarean section bc obstructed. -rarely does brow presentation corrects spontaenously bc hypotonia cant flex the head

Shoulder dystocicia (prolonged labour)

8% of all maternal deaths due to obstructed labour. -prolonged labour means prolonged length of stage 1 and stage 2. Active stage 1: -primi gravidia: >1cm /hr -multigravida: >1.5cm/hr Stage 2: Time: -primip > 2 hrs -multi >1 hr Obstructed labour: despite strong contractions of uterus > fetus cant descend through pelvis (primarily malpresentation/malposition) Cephalopelvic disproportion: -fetal head is disproportionate to the pelvic canal and will become obstructed. -may be A. Marginal: moulding of fetal head > delivery may be possible B. Definite: pelvis is too small or fetal head is too large and surgery is needed

Secondary PPH:

>500ml within 24-6 weeks post partum Etiology: 1. Post partum endometritis: -secondary infection of placental site or endometrium post partum. Causes inflammation > bleeding -Baseline bloods PLUS AMG: ampicillin, metronidizole, gentamycin 2. Submucosal fibroid: may be damaged during delivery > bleeding. -BL bloods PLUS US +/- surgical removal >>hysterectomy 3. Choriocarcinoma: malignant tumor via trophoblast of embryo that invades into the placenta >> produces BHCG -BL bloods PLUS serum BHCG to rule out gestational trophoblastic disease and continued BHCG production affter pregnancy

Mulitple pregnancy risks

Antenatal: -anemia: ^ rx of mom becoming anemic > need iron supps -Pre-eclampsia and Eclampsia: larger placental tissue > ^ rx of pre eclampsia >> need low dose aspirin -APH: ^ rx of placental abruptioin and vasa previa -GDM -MSK pain due to weight on lower back -IUGR: due to ^ need of vascular demand Perinatal (close to birth and after birth): -cord prolapse -cesarean section -PPROM and Preterm biirth Post natal: -PPH -Post natal depression Monochorionic twins specific risks: -cord entanglement (McMa): Mx: early delivery by cesearean, daily CTGs looking for severe variable decelerations -co-twin death: death of 1 twin >> hypotensive insult in other twin. Death of A > 25% chance of death in B + hypoxia >> cerebral palsy in B -selective IUGR: Significant discordance btwn the babies. > 20% means selective IUGR. Doubles rx of fetal death> delivery warranted -Twin-Twin transfusion syndrome (TTTS) TTTS: in monochroionic twins have direct communication btwn vessels from umbilical cord of twin A and twin B: -Arterial to arterial or venous to venous > no problem -Arterial and venous > BAD when in excess: get NET movement from arterial circulation of one fetus to venous of another => Donor twin: losing circulatory volume > becomes hypovolemic, hypotensive, anuric and thus anhydramnios => Recipient twin: becomes flooded > >hypervolemic leading to high output cardiac failure and polyhydramnios -Untreated >95% fetal mortality > ^ in fetal loss from 14-22 weeks compared to dizygotic twins. -Rx of loss increases around 22 weeks and again at 34 weeks thus like to deliver pre-term TTTS TX: laser photocoagulation of placental vessels LPCV -performed at around 19weeks -TTTS monochoronionic twins > fetal biometry every 2 weeks from start of second trimester 12 weeks plus weekly CTG from 32 weeks. Fetal mortality: intra uterine death: One of the rxs of carrying twins is that there is an increased chance of fetal mortality: -death to monochorionic twin is hazardous > immeidate delivery -death of dichorionic twin > no need for immediate delivery unless pathological > Pre eclampsia, infection, IUGR Free fetal DNA testing: screening is possible in monozygotic twins bc there is only 1 set of DNA. -In Dizygotic twins > there r 2 sets of DAN > thus screening is not valid. Screening > combined first trimester screening: -Dizygotic twins: either one or the other may have Downs syndrome -monozygotic twins: either both or neither wil have genetic abnormality. Nuchal translucency allows individual rx to be calculated for each baby Dx testing: -dizygotic wins: amniocentesis or CVS needs to be done for both but in monozygotic > need 1 sample taken *IUGR: <10th centile + fts of growth restriction for gestational age: -see this in dichorionic twins where there r 2 placentas Recomendation: 3rd trimester 24 weeks > monthly fetal biometry/growth US -week 32 > weekly CTG Risk specific to monochor

Bishop score

Assesses cervix to see how soon you may go into labour and if IOL is required. -A score to tell us the likelihood of a successful induction of labor (painful, regular contraction causing dilatio and effacement of cervix). A VE is required to assess station, dilation, effacement, consistency and position of cervix. Bishop score: score out of 13 -score of 0 to 5: cervix is still firm and tightly closed. -Score >8: body is ready for labour Modified Bishop score: score out of 10 -Score of <8 : cervical ripening is required before IOL (e.g. Cervidil/foley balloon catheter) -Score of 8 or more: IOL is appropriate without the need for ripening When do you need to do cervical ripening? Bishop score <8. -If u give prostaglandins when bishop shows a favorable cervix > increases rx of hyperstimulation and precipitate labour -Ripening of cervix is what BS is trying to assess: A. Dilation: approaching 3-4 cm B. Effacement: shortening of cervix length C. Softening of cervix D. Position: anterior is favorable Cervical ripening is carried out eithher: 1. Mechanicaly: Foley balloon catheter 2. Pharmacol > prostaglandin therapy (cervidil) *important: these mechanisms r capable of inducing labour. But thhe main aim is to prepare cervix for an ARM and or oxytoci ninduced labour. Must begin continuous cardiac monitoring to look for signs of fetal compromise and uterine hyperstimulation

Screening tests for chromosomal abnormalities

Combined first trimester screening (4): 11-13+6 weeks -MA + BHCG + PAPP A + Nuchal translucency test Down syndrome: ^ Maternal age (MA), ^ BHCG, Low PAPP A, ^ Nuchal thickness in T21 Quadruple test: 15-20 weeks -Maternal age + - AFP (Low in T21) + unconjugated Estrodiol + (Low in T21) + Free BHCG (^ in T21) + Inhibin (^ in T21). *put in order A-> Z, it is low, low, then high, high. Cell free DNA screening: 10 weeks -screen maternal serum plasma: very high sensitivity (99%) and specificity (99%) but costs $450 Diagnostic tests: 1. Chorionic Villus Sampling: 11-13 weeks > goes well with combined first trimester screening: ~12 weeks. -a/w ^ rx of transverse limb reduction defects when conducted before week 10 > risk of miscarriage Risks: -Infection -RH sensitization: babies blood may enter mothers and sensitizes RH- mom -Miscarriage: 1% > 1 in 100: higher risk than amniocentesis 2. Amniocentesis: 15-20 weeks: -^ed risk of talipes when conducted before 14 weeks and when compared to CVS > results may be invalid slighly more often. Risk: 1. Infection 2. Miscarriage: 1 in 200 3. RH sensitization 4. Amniotic fluid leak Post natal Dx: -rapid fluoresent in situ hybridization for trisomy 21: blood sample sent for karyotyping and confirmation of trisomy 21.

Benefits and challeneges of breast feeding

Benefits: -post partum bleeding reduction (due to oxytocin stimulation > contractions uterine myomyetrium and breast myoepthelial cells) -weight loss: due to removal of milk -decrease risk of cancer: breast feeding is protective against breast and ovarian cancers -cheap -convienent -mild contraceptive benefit: women who had CS > need 12 months before having another baby -gratifying: decreases rx of PND: post natal depression For the baby: -infection prevention: IgA antibody is transferred to baby>> ^ protection against respiratory tract, ear, and GIT infections in teh first 6 months during immune development. -autoimmune disease prevention: aids neonatal immune system -decreased atopy -obesity and T2DM protection -GIT development: epidermal growth factor in breast milk aids development and may protect against lactose intolerance -neurodevelopmental benefit Challenges: -discomfort: sore nipples. Solution: -alternate nipples or express to allow them to heal -lactation consult -time restriction on moms and impact on work bc they have to always breast feed: solution: A. Expression milk in bottles > can be stored until next feed. Storage: Bench: 3 hours Fridge: 3 days Freezer: 3 months > rewarm in hot water not microwave -ensures that milk proudction doesnt stop Contraindications: -cannabis (marijuanna) use: accumulate in breast milk > a/w neurodevelopmental changes in baby -HIV: C/I -maternal infections: HBV/HCV are only at risk of transmission if nipple is cracked and bleeding -chemo or immunosuppressive maternal therapy

Urinary incontinence Ix

Bladder diary- 2-3 day period to record times of micturition and her voided volumes w/ sxms. Fluid intake also reocrded -Urinalysis: MCS -Post void residual volume scan: ultrasound scan ass for voiding dyfunction a/w overflow incontinence -cytoscopy -dye test (if urinary tract fistula suspected) -urodynamics if uncertain dx or faifl to respond to therapy, or need surgery

Blood types and RH

Blood types: -A: has antibody B. >> receive blood A or O -B: has antibody A >> B or O -AB: has no antibody >> A, B, AB, O: universal recipient -O: has antibody A and B. > universal donor but only can recieve blood type O. Rhesus gene is DOMINANT and gets one Rhesus allele from mom and one from dad. ABO blood group inheritance: A and B are both dominant while O is recessive. Thus: -A and B parents gives AB blood group -A and O gives A blood group Pathophys: -Fetus is Rh+ and mom is Rh- > mom creates antibodies to antigens on babies red cells > mediate hemolysis in fetal circulation in next baby. ABO incompatibility is way more common than Rhesus but only causes very mild hemolysis. This leadst o post natal jaundice. Only occurs in an O mother and an A or B baby.

Anormal uterine bleeding: IPALM uterus anovulatory PM systemic CHAT

Can be: 1. In the uterus -IPALM: infection, polyp, adenomyosis, leiomyoma, malignancy 2. Anovulatory: PM: PCOS, menarche and menopause 3. Systemic: CHAT: contraceptives, hematological (VWD), Anticoagulants, thyroid HX: 1. Normal cycle? 21-35 is normal. >35 days is oligomenorrea (infreq menstruation) 2. Normal days of bleeding? 3-7 is normal 3. R they regular? Painful? 4. When is bleedign worse? During or between periods (pathology) or after sex? 5. HOw much? How many pads do u use per day? Change >3 hours is indicator of heavy 6. Do you leak? Do u wear pads super pads or both? Complications: look for Fe def anemia: r u cold, tired, increase in heart rate, light headedness and dizzy?

Jaundice in pregnancy

Common preg associated causes: 1. Acute fatty liver of pregnancy: -rare cx which may occur in 3rd trimester. Fts: -abdo pain -N/V -Headache -jaudnice -hypoglycemia -severe disease may result in pre-eclampsia ix: ALT is elevated 500u/L MX; -supportive mx until delivery 2. Intrahepatic cholestasis of pregnancy: -AKA obstetric cholestatsis occurs in 1% of preg and seen in 3rd trimester. -Most common liver disease of pregnancy -bile duct >obstruct > conjugated hyperbilirubinemia >> jaundice and pruritus Fts: -pruritus > palms and soles -no rash -raised conjugated bilirubin Mx: -ursodeoxycholic acid > sxmopatic relief -typically induced at 37 weeks Cxs: -^ rate of still birth thus require immediate delivery Other causes: 1. HELLP syndrome 2. Gilbert's Syndrome: exacerbated by pregnancy 3. Acute hepatitis

CTG: DR C BraVADO

D: Details: pt name, DOB, date, time, stage of labour R: risk: is this a high rx pregnancy? Any major antenatal cxs? C: contractions: rate of contractions per minute: tachysystole: >5 in 10 min for 30 min. Hypertonus: contraction lasting >2 minutes Bra: baseline rate: Normal: 110-160. Brady <110. Tachy >160 V: variability: <3 absent, 3-5 reduced, 6-25 normal, >25 increased variability A: Accelerations > 15bpm >15 seconds D: decelerations >15bpm >15 seconds -Early U shape -Late: V shape -Variable: V/W shape -O: summary and DDX Abnormal CTG: -to Dx fetal hypoxia > get fetal blood sample and test pH and lactate. A. pH: w/ increasing hypoxia and hypercapnia the pH decreases: acidosis B. Lactate: w/ increasing anerobic respiration > lactate rises. *CTG is only indicative and not diagnostic. -A fetal scalp blood is taken to get an assessment of these values: CTG is only effective at reducing fetal mortality when combined w/ fetal lactate. PH sampling: >7.25: repeat after 1 hour 7.21-7.24 : repeat in 30 minutes or consider delivery if significant fall has occured <7.2: delivery is indicated: indicates fetal hypoxia: high CO2 in the fetal blood. *Adult: 7.35 —> 7.45 Fetus: normal is >7.25 Lactate sampling results: <4.2 mmol/L : normal 4.2-4.8: pre-acidemia > repeat in 30 mins or consider delivery 4.8: acidemia: delivery is indicated. ************** Deliver when pH <7.2 and when lactate levels are >4.8. (Normal lactate is <4.2).

Perineal tears

Degree of tears: 1st degree: superficial damage w/ no muscles invovled 2nd degree > perineal muscle tear 3rd degree > perineal muscle tear + anal sphincter tear -3a: <50% of EAS tear -3b: >50% of EAS tear -3c. Internal anal sphincter tear 4th degree tear: perineal muscle tear + anal sphincter external and internal tear. RFs: -primigravidia -large babies -precipitant labour -shoulder dystocia -forceps delivery Prevention: -episiotomy upon crowning of baby Mx: -suture

Stage 3: <1 hour duration

Delivery of the placent Prevention of PPH: -rub uterus -continual cord traction CCT is applied gently to placenta until >detachment >> gush of blood, sensation of detachment. -placenta can be delivered adn twisted upon leaving the vagina to ensure no retained products remain in cavity. -If palcenta is allowed to be delivered w/ normal contracts (physiological mx) > much higher incidence of blood loss and post partum cxs. Mx: -Give Oxytocic Injection > contracts myometrium > prevent excessive bleeding PPH. *PPH is largest cause of maternal morbidity and active mx > oxytocic compared to phyisological mx (giving nothing) reduces rx 4x What is used? 1. Oxytocin: 10 units IM or IV (must know this) -fast acting 20-30 seconds -short half life of 20 mins. -SE: hypotension: oxy low sin, N/V/ headache 2. Ergometrine: -slower onset but loner lasting 60 mins -rarely used -SE: hypertension + N/V/ headache 3. Oxytocin-ergometrine combination: syntometerine -decreases rx of small PPH btween 500-1000ml but not over 1000ml AE: hypertension N/V?headache Cord clamping: -blood is taken from the arterial and venous circulation: -measures lactate and pH levels: a measure of amount of anerobic respiration and thus hypoxia in the fetus during delivery -baby blood group: esp in RH - mom. Delivery of placenta: -retaiend placenta occurs if this process takes >1 hour. ***Duuration: anyone <1 hour.

Consent for Cesarean section: IPBRAAD:

Indication: -Hi im Ali. -Have you had a CS before? -How much do you know about CS? 30% of deliveries are done by CS -CS is a surgical technique where baby is delivered via incision in the uterus. Very clear indications: -most common indications include: 1. Antepartum hemorrhage: such as placenta abruption or placenta previa which are most common causes of antenatal bleeding and when severe may warrant CS 2. Severe pre-eclampsia: rx of maternal health arise 3. Chorioamnionitis: dx warrants immediate CS due to rx to maternal and fetal health 4. Fetal distress 5. Twins > need CS Procedure: Before: -if CS is planned/elective: most common at 39 weeks -Fasting the night before -Anesatist will come speak to you and will give: spinal anesthetic: needle is inserted after numbing the area with local anesthetic > get complete paralysis from waist down: sensory and motor. During: -*at ~36 w > lower fibrous segment of uterus forms > has less vasculature and active muscle tissue; Lower uterine segment cesarean section: 98% of time > horizontal cut made along top of bikini line -baby and the placenta will be delivered and will be able to say quick hello before baby is taken to be cleaned and cord cut properly. -Delivery takes about 5 minutes, and stitching may take about half an hour. -once clean, dry and warm > baby can brought back in > skin to skin contact Classical cesarean section 2%: vertical cut: occur in significant prematurity (when lower uterine segment has not completely formed) -due to cut in to the highly vascular upper segment > ^ rx of uterine rupture in other preg: both antenatally and during spontaneeous labour. For this reason that next pregnancies > will get classical cesarean again. (Give antibiotics on incision site, antacids to prevent aspiration of stomach contents) Afer: -recovery room: stay in post op room for few hours to monitor any cxs: 1-2 hours -IDC: due to the spinal anesthetic > pt will not mobilize well for several hours and IDC is inserted. -Day 1: get up and move around to prevent DVT -thromboembolism prophylaxis: stockings +/- LMWH (clexane) -analgesia: paracetamol/NSAIDS -Discharge Day 3-4 home Benefits: -faster than vaginal delivery -less pain than labour -similar risks to normal vaginal delivery -hysterectomy and tubal ligation can occur as well Risks: -If we collected 100 healthy preg women and delivered via CS > 16 of them would have some form of complication. 16/100 > cx. -pain and slow recovery: 3-4 days vs vaginal (1-2 days) -bleeding -infection -damage to local structures: bladder, bowel, utreter, uterus -although very rare: we do need to tell u that emergency hysterectomy is a risk of CS -thromboembolism (post op > move u around to reduce risk of getting clots in le which can go to lungs) -anesthetic risk: allergic rxn -risk of uterine rupture or placental attachment abnormalities due to the cesarean scar in next pregnancies. *vaginal births r still possible after a CS. Repeat CS is 1 in 4. Alternatives: -vaginal delivery: can opt for vaginal delivery and attempt for VD if no cxs Any questions? Document and consent

Station of intramental delivery

Difficulty of intramental delivery is by station of baby. +5: outlet statiotn: head seen: Also called a lift out station and suitable for forceps +3> +5: low station: >+3 in absence of fetal scalp molding > forceps 0 to +3: mid cavity station: sits just below ischial spine > take to theater for a trial of forceps +/- rotation. May need CS <0: high station: cant do instrumental Types of forceps: 1. Neville Barns: main forcep used for instrumental delivery w/ large cephalic and pelvic curves 2. Keiland's: a forcep primarily deisgned for roation of the head thus the pelvic curve is minimal. Not currently recommended. *Neville barns > standard forcep deliveries and Keilands for rotation Ventouse: -plastic cup is applied near the occiput to maintain flexsion during traction and a vaccuum is creaed inside the cup using a suction pump. Common form > kiwi forcep: place it on anterior part of posterior fontanelle > suction forms a "chignon"

CTG trace:

FHR: Normal: 110-160 Variability: looking at presence of hypoxia: any form of O2 depreiv > ^ SNS tone >> ^HR Absent: <3 Reduced 3-5 Normal: 6-25 bpm Increase >25 Accelerations: sign of normal oxygenation: >15bpm for >15 seconds -> termed reactive trace -prolonged acceleration: 2min > 10 mins Anything longer than 10 min is a shift in the baseline Decelerations: Decrease >15 bpm for >15 seconds: 3 main types: A. Early deceleration: head compression -starts when uterine contract and recovers when contractions stop -***EURLY deceleration: U shape rather than V. B. Late deceleration: fetal hypoxia >> placental insufficiency. -begins at the peak of the contraction and recovers after contraction ends. U shape rather than V. -due to insuff blood flow > blood flow to fetus is reduced causin fetal hypoxia and acidosis . -following late decel > fetal scalp lactate may be indicated to look for fetal distress Pathology: maternal hypotension, PET, uterine hyperstimulation C. Variable: cord compression: rapid onset and recovery > looks like V or W w/ contractions -rapid fall in H w/ variable recovery phase. -more V shape. ***remember: cord compression >>variable decel Pathology: cord compression D. Sinusoidal pattern > Severe fetal pathology -high a/w fetal morbidity and mortality -smooth regular wave like pattern, 2-4 cycles a minute, w/ BL at around 120-160 *Immediate intervention is required Pathology: fetal anemia, maternal fetal hemorrhage.

Cephalic presenations continued

Face presentation OP: max amount of deflexion (extension) of fetal head -most favorable of the abnormal cephalic presentation in terms of birthing cx -deflexsion has gone so far that the submentobregmatic diameter 9.5cm presents which is similar to normal vertex SOB 9.5cm -1 in 800 babies Aetiology: -lack of flexor tone +/- exaggerated extensor tone -neck mass: ie enlarge thyroid -anencephaly: presents w/ face position bc of lack of clavarium (underdeveloped brain and incomplete skull) Dx: due to anencephaly or neck mass or ^ extensor tone may be dx on US. Antenatally but more commonly found on VE VE > palpable face. Easy to ocnfuse w/ breech presentation. Irregular shape Mx of face presentation: extensor activity in the OP position -1st stage: consider cesarean section -2nd stage: closely mmonitored vaginal delivery -fetal head can come out disfigured but reassurance of parents that this will resolve w/in 24 hours. Continue fetal monitoring: avoid fetal scalp clip bc u will jam it in the face. Breech presentation: -bottom caudal pole of baby presents in inlet. 3 ways: 1. Frank breech: legs extended up beside the head 2. Complete breech: legs r flexed besides the body > sitting cross legged 3. Footling breech: legs out the cervix Incidence: 4% of births Predisposing factors that promote breech/transverse presentations: -multiple pregnancy: causes abnormal psoitioning -fetal anomaly -fibroids: obstruction to rotaiton -polyhydramnios: ^ distension of uterus making it easier to rotate -^ parity: uterus and ant abdo wall lack tone -placenta previa Ix: US. Mx: >37 weeks not in labour: 1. External cephalic version: presenting legs/buts is changed so that head presents first 2. Tocolytics: to prevent labour (salbutamol) 3. Anti D 4. Elective CS or vaginal delivery: CS at 39 weeks has shown to decrease mortality significiantly compared to vaginal delivery >37 in labour: 1st line: Cesarean section + Anti D 2nd line: vaginal breech delivery + Anti D 3rd line: ECV: external cephalic version + Anti D External cephalic version > Adverse effects: A.feto-maternal hemorrhage due to placental abruption or uterine rupture. Thus must remember to give ANTI-D where appropriate. B. Cord entanglement -Plan for elective CS CI: -footling breech: leg out of cervix -antepartum hemorrhage -previous CS scar -twins -placental abnormalities -hyperextension of fetal head. Procedure is only indicated when: -term >37 to 39 weeks. 40 or more > need CS -vaginal delivery is desired over CS -legs in flexsion (frank) -singleton pregnancy Success rate: 60%, harder in obese females, nulliparous Complications of breech vaginal deliver: -cord prolapse -placenta abruption -PROM: pre-labour rupture of membranes -perinatal mortality -fetal distress <100bpm -preterm delivery -lower fetal weight Cx of cesarean section: -PE -Infection -Bleeding -bladder/bowel trauma -slow recovery -longer hospital stay -delayed bonding and breast feeding -increased rx of repeat CS, infertility, uterine rupture, placenta accreta/abruption CIs: -large fetus > 3.8kg -small fetus: IUGR babies should be delivered by CS bc they cant w/stand strain of delivery -placental insufficiency > need CS -footling breech: where the leg is near the cervix

Infertility

Failure to concieve after 12 months of UPSI -primary: never been pregnant -secondary: pregnant before Unprotected sex: 1/6 chance of getting pregnant *Within 1 year of trying, 85% will become pregnant Epi: -15% of couples experience infertility Aetiology: -Male cause: 1/3 -Female cause: 1/3 -combination: 1/3 Male factors: 1. Has partner fathered kids before? 2. Occupation 3. Has he had semen analysis? 4. History of mumps? Exam: look for testicals bilatearlly, shape and size of each testis, absence of redness/swelling in testicles/penis plus absence of d/c to suggest an STI Hypogonatotropic hypogonadism: gonadal failure do to absent or low levels of GnRH: 1. Do you know you BMI? -Low body weight > Leptin from adipose tissue play a role in promoting FSH and LH > allow ovulation 2. Excessive exercise or strict diet? -hypothalamus down regulates GnRH > thus no FSH >> no ovulation 3. Major stressors? -stress a/w infertility. 4. Have you had a complicated labour? Post partum hemorrhage? -Sheehan's syndrome: Post partum hemorrhage (bleeding) following delivery can significantly reduce the circulating blood volume > pituitary is the first to experience ischemia and infarction. 5. Galactorrhea (spontaneous flow of milk w/o pregnancy)? Or visual trouble in lateral regions of vision? -PRL is secreted from posterior pituitary > controls production of milk after pregnancy. PRL also inhibits ovulation (period) while you are breastfeeding. -Ectopic PRL (from an adenomatous tumor) may cause inhibition of ovulation and infertility. Adenoma: w/in pituitary may inhibit FSH and LH preventing ovulation and causing infertility.

Fetal growth and well being assessment:

Fetal growth: 1. Fundal height assessment: -measure from pubic symphysis (pubic bone ) to top of uterus > should match gestational age to within 2cm after 20 weeks. Ex: if 24 weeks: fundal height should be between 22-26 cm. 2. Fetal Biometry: (fetal size): -biparietal distance BPD/Head circumference HC -Abdominal circumference AC -Femur length FL -estimated fetal weight > gives indicator for small for gestational age baby (<10th centile) Fetal well being: When baby is small for dates in the 22w biometry scan do more detailed analysis of individual components of fetal biometry: 1. abdo circumference: gives impression of fat and glycogen store. 2. biparietal distance vs abdo circumference in the biometry: Symmetrical IUGR: Causes: chrom anomalies trisomy 13,18,21, TORCH infections, fetal alcohol, Smoking, OH, Nictotine -affects baby systemically independent of fetal suppy. -Presents in early stages of gestation ***Symmetrical IUGR is defined by: Both AC and BPD <10th centile with <2 weeks between them. Assymtrical IUGR: Causes: Placental insufficiency: poor supply to the baby > either via placental or hypoxia/hypoperfusion -placental insuff > fetal hypoxia > stimulates compensation to restore blood flow to vital organs thus blood redirected from peripheries and abdomen to the head. *Assymetrical IUGR > head and brain enlarge at a faster rate than the abdomen Defined by: estimated gestation for HC >2 weeks that of the AC -Abdo circumference <10th centile Amniotic fluid index: -during US, 4 pockets of amniotic fluid is measured and an estimated total liquor volume is estimated: -represents fetal perfusion: blood is filtered from kidneys > urinated out into amniotic fliuld > baby swallows it and the balance of fluid continues. - Poor fetal circulation > blood is directed AWAY from kidneys thus less output of urine >>total amniotic fluid volume decreases Biophysical profile: when biometry (growth size) suggests IUGR > send for BPP: assess 5 things: 1. Fetal breathing rate 2. Fetal movement 3. Fetal tone 4. Amniotic fluid index AFI 5. CTG Each scored out of 2 to give total score of 10. >7 is health baby. Fetal dopler US: Umbilical Artery Doppler: -Normal: shows systolic (peaks) and diastolic (downward slope) -Pathological: sharp peaks (systolic) then flat line then sharp peak then flat line -stopped flow: the diastolic flow touches the zero line -reverse flow: diastolic line is below the zero line. MCA doppler: assess fetal cardiovascular distress, anemia, hypoxia: used as an additional work up of IUGR baby, -analysis of middle cerebral artery: -normal: fetal MCA has high resistance flow: less anterograde flow in fetal diastole -Pathological: turn into low ressitance flow > due to fetal head sparing Fetal movements: ask if present, increasing or decreasing

Menstural phase of the Follicular phase

First phase: Follicular phase: menses and proliferative phase Second phase: Luteal phase: secretory phase (progesterone) Menses: 3-7 days. Uterus: -In fertilization: trophoblast layer of blastocyst produces hCG (human chorionic gonadotropin) > this allows corpus luteum to keep functioning to be able to produce PROGESTERONE. -If no fertilization: no hCG thus corpus luteum involutes > becomes corpus albicans (fibrous non fucntional tissue) -No corpus luteum > thus no progesterone > thus get constriction of spiral arteries that supply the stratum functionalis of the endometrium (this is the poriton that becomes vascularizes and sloughes off during menses) > causes ischemia and detachment (menses). -Stratum basalis (basement layer) of endometrium is maintained. Ovary: 1. Pulsatility of GnRH is slow thus get FSH stimulated in ant. Pit (AP). FSH stimulates the follicle -Primary folllicle: oocyte -The secondary oocyte (haploid) initiates meiosis 2 but halts at metaphase 2 until fertilization occurs. If it doesnt occur > doesnt progress and get menses. -By puberty, they have 400, 000 follicles from the 1 million follicles they at from birth. Pre-Antral Follicle: 1. FSH stimulates 10-12 primary follicles into secondary follicles. When a primary follicle is stim > releases Anti-Mullerian Hormone (AMH) > inhibits development of other primary follicles. Only about 6-12 replicate fast enough before being suppressed. -Younger females: have more follicles replicatign thus need higher AMH to stop folilcles from progressing thus represents fertility -^ FSH causes granulosa cells to convert androgen to estrogen to form Pre Antral or thecal follicle: 2 layers: 1. Theca interna > produces androgens 2. Theca externa > capsule of the developing follicle Theca cells plus granulosa cells help form the corpus luteum.

Male infertility:

Infertility is abnormal semen parameters in a couple who is unable to conceieve after 1 year of unprotected sex -WHO defines it as 1 or more abnormality in semen analysis or presence of inadequate sexual/ejaculatory function ' RFs: 1. Varicocele (dilation of veins of pampiniform plexus of scrotum). Occur commonly on left side. 2. Cryptorchidism: undesended testis a/w oligozoospermia, hypospadias, and testicular cancer 3. Prior chemotherapy/radiotherapy: transient or permanent loss of spermatogenesis. (Alkylating agents > cyclophosphamide r harmful) 4. Testosterone supplementation or anabolic steroids inhibit spermatogenesis, antifungals (sulphasalazine affect spermatogenesis), (antipsychotics, antidepressants, antihypertensives: cause retrograde ejaculation) 5. Cystic fibrosis and congenital bilateral absence of vas deferens 6. Klinefelters syndrome (47 XXY) 7. Endocrinopathy a/w low testosterone or low FSH/LH: these include > hyperprolactinemia, gonadotrophin (FSH/LH) def, genetic conditions > Kallman's syndrome > hypogonadism due to def in gnRH. 8. Previous infertility: couldnt had child previously. Hx: 1. Inability to conceive 2. Vasectomy 3. Palpable and dilated testicular veins (varicocele is most common abnormality a/w male infertility!!!!!) 4. Erectile dysfunction 5. Testis atrophy 6. Pain, blood, pus w/ ejaculation > prostatitis or epidymitis Epi: -1 in 6 couples have difficulty conceiving. -male factor alone is responsible for 20% of the cases. Aetiology: 1. Abnormal spermatogenesis (sperm production): most common and unknown etiology. Low testosterone is due to obesity, endocrineopathy and medicines. Others: varicocele, increased scrotal heat, smoking, undesended testis, alcohol. 2. Reproductive tract obstruction: may be congenital > bilateral absence of vas deferens related to cystic fibrosis. Also, vasectomy. 3. Erectile dysfunction: may be a/w diabetes 4. Impaired sperm motility: reduced in kartagener's syndrome or in antisperm antibodies. Pathophys: -testosterone is produced by testicular Leydig cells (L for LH) by LH hormone. -Spermatogenesis is controlled by testosteone and FSH. FSH > sertoli cells > support spermatogenesis in the seminiferous tubules. -GnRH and FSH is negatively controled by testosterone (T) and through aromatization to estrodiol at central/peripheral levels. -inhibin is produced by sertoli cells > negative effect on FSH. -Circulating testosterone is bound to sex hormone binding globulin SHBG and albumin. Levels of SHBG affect active portion of circulating T or free T. -Hyperprolactinemia has a negative affect on GnRH secretion. Ix: 1. Semen analysis: measures sperm concentration (<15 million/ml), motility (<40% motile), mophology, volume and ocnsistency. 2. ASA: Antisperm Antibodies: IgG, IgM, and IgA titres Mx: 1. GnRH deficiency (Low FSH/LH) or unexplained male infertility>> Chorionic gonadotrophin (hCG) or pulsatile GnRH A. Men with secondary hypogonadism such as gonadotrophi def or genetic conditions (kallman syndrome) give gonatotrophins or pulsatile GnRH. B. hCG and follitropin alfa (FSH) increases sperm production 2. Hyperprolactinemia due to pituitary adenoma: High prolactin > inhibit GnRH (FSH/LH) A. Men with secondary hypogonadism due to hyperprolactinemia from pituitary tumor > tx with bromocriptine 3. Presence of antisperm antibodies > Tx w/ intra-uterine insemination or IVF (ART: assisted reproductive techniques) 4. Varicocele: Tx > surgery > percutaneous embolisation

Menstruation cycle:

Follicular (menses, proliferative phase) then luteal phase (secretory phase). Foliuclar phase Luteal phase Menses proliferative phase. Secretory phase -Follows in Alphabetical order. 1. GnRH slow pulsatile release FSH from AP > stimulates 6-12 follicles 2. High FSH stimulates follicules > granulosa cells produce Est 3. ^ Est has neg feedback on GnRH and FSH at first 4. Very high Est causes a positive feedback at day 14 where it causes fast pulsatile GnRH > get LH surge and FSH spike > ovulation 5. LH surge > ovulation > follicle ruptures and egg is released 6. Follicle becomes corpus luteum > produces Progesterone for 14 days. If fertilized > the trophoblast of blastocyst produces HCG which maintains corpus luteum > produces progesterone longer. -If not pregnant, after 14 days > corpus luteum > corpus albicans > no more progesterone made > get ischemia of stratum functionalis of endometrium > menses. 7. Progesterone causes endometrium to be vascular and glandular *PE increases core temperature to promote fertilization

Forceps vs ventouse

Forceps: maternal trauma, less fetal trauma (skull fracture and subgaleal hematoma r very rare), analgesia required (regional/epidural), very low failure rate. -CI: non OA position. Ventouse: less maternal trauma, more fetal trauma (slight higher risk of subgaleal hematoma but less rx of skull fracture), need local. -CI: face presentations, preterm <34w. -failure rate is slightly more bc suction may not stick esp if baby is moulding

Pelvic Pain DDX and IX

GIT: -Appendicitis: periumbilical then RIF migration? N/V LOA -Diverticulitis: constipation, worse on straining, Bleeding, F/R/N -IBD: episodic diarrhea and constipation, frank blood or mucus in stool, changes in joints, skin, eyes? Renal: -renal stones (nephrolithiasis): loin to groin colicky pain. Cant lie still and very severe -UTI/pyelonephritis: burning/stinging urine, frequncy, smelly/cloudy urine, flank pain? Uterine: -enodmetriosis, adenomyosis -leiomyoma (fibroid): *heavy period, painful period, spotting? -malignancy: gradual onset of continuous pain? Post menopausal bleeding? Common in post menopausal fat women -asherman's syndrome: synechia: adhesions w/in uterine cavity can mediate pain. * Uterine surgery, gradual onset pain? Dyspareunia? Tubal: -PID: Last STI check? Dyspareunia, d/c or spotting? F/R/N -Ectopic: sudden peritonism, NV, shock: presyncope and cold? Ovarian: -cyst: can rupture. Sudden onset unilateral pain? Continually decreasing? N/V? -torsion: sudden onset unilateral pain, colicky pain, peritonism -malignancy : gradual onset, weight loss, vaginal bleeding or d/c IX: 1. First pass urine and vaginal swab: gonorrhea/Chlamydia infections 2. B-HCG test: normally it doubles its level every 48 hours. Stable or slow decline > ectopic. Decreasing > miscarriage 3. Vitals: for shock in ectopic: High HR, Low BP -FBE raised WCC w/ neutrophils 4. transvaginal and abdominal ultrasound 5. Hysteroscopy or laperoscopy

Bishop score 8 or greater > do IOL

Go straght to ARM or Oxytocin infusion if Bishop score is 8 or greater: 1. ARM: artificial rupture of membranes: -liquor contains endogenous prostaglandin that both directly augments uterine muscular activity and ^'s receptivity to oxytocin. -following arm > contraction will exert more pressure on fundal pole (top) of fetus forcing the presenting part down against the cervix > assist mechanically with cervical dilation and via the ferguson reflex (valsalva) will promote endogenous oxytocin release Rxs: -chorioamnionitis: prophylactic benzylpenicillin given when membranes rupture for >18 hours -cord prolapse: down w/ the membranes but more likely when we induce labour before head is engage (plugs the hole) Benefits: -shorter labour duration than oxytocin, reduction of labor dystocia bc the waters r broken which promote better labor. 2. Oxytocin infusion: Syntocinon -in majority of cases, this will follow an ARM -general dosing is 10 units per liter of Hartmans IV at 12ml/hr. Slowly titer up until u get good uterine contractions. (This is the same dose as active mx in 3rd stage of labour) Rxs: -uterine hyperstimulation: >6 contractions in 10 minutes -hypotension: syntometerine contains ergometrine > causes hypertension and may balance this out. -fluid retention: hyponatremia in rare cases -PPH > exogenous oxytocic medications cause negative feedback on receptor thus decreasing response to oxytocin in the active 3rd stage mx of labour > thus infusion recommended to be continued for an hour after deliver to prevent uterine atony. Benefits: -effective augmentation of latent first stage -effective mx following arm ***Risks for IOL 1. Inducing too early 2. The Particular method used 3. Fail > thus may need CS

Group B streptococcus (Strep Agalactica): B for Benzyl PeniCillin: C for clindamycin

Gram +: Alpha > strep viridans and strep pneumonia Beta hemolytic: Group A: strep pyoenes, group B: strep agalacticae Gamma: enteroccus GBS is part of normal flora of genital tract in 10-30% of wmen in Aus and may cause asymptomatic bacteruria. -During delivery, 70% of women who have GBS will pass bacteria on to their baby -.4% of cases > can cause mild pneumonia w/in first 7 days of life and may even cause neonatal meningitis *36 weeks just before term > vaginal and anal swab is taken for > GBS Matneral infection: -asymptomatic bc part of normal flora Asymptomatic bacteuria: a/w ^ rx of transmission compared to vaginal flora. Rx: -Preterm Prelabour rupture of membrane PPROM and preterm labour > reason for PPROM is bacterial mediated inflam -post partum endometritis Fetal cx: -fetal sepsis: contraction occurs via vaginal delivery >> lead to neonatal pneumonia and meningitis Obstetric risk factors: > give intrapartum chemoprophylaxis. -previous infant w/ GBS -GBS bacteriuria -spontaneous onset of labor <37 weeks -rupture of membranes >17 hours -Intrapartum fever 38 or more. Mx: -36 week anovaginal swab > check for GBS -intrapartum: IV Benzylpenicillin or Clindamycin in penicillin sensitive pts -In PPROM u r going to be giving erythromycin TDS for 10 days to prevent Chorioamnionitis

Best type of pelvis for birth

Gynecoid is wide and allows birth Android is narrow and more difficult

Hepatitis B

Hep B > DNA virus infects hepatocytes and is mainly transmitted via bodily fluids semen, vaginal secretions and saliva, maternal) 3 fundamentals for Hep B serology: 1. HBsAg: presence of viral particles NOW 2. Anti-HBsAg: immunity or cleared 3. Anti HbcAg: presence of viral particles EVER Worry about acute infection w/ high viral load that may transmit to baby: looks like this: 1. HbsAg (NOW): positive 2. Anti HBsAg: (imunity/cleared): negative 3. Anti HBcAg (presence of viral particles EVER): positive High rx of transmisison to fetus when mother is infected 50% of ppl dont know they r affected and mx of labour is altered to prevent blood to blood contact NIRS Mx: NIRS mx of all infections in pregnancy: -Notify and follow up as high risk -Infectious disease referal Reduce vertical transmission or react w/ mx Baby: no rx to fetal survival and need for immediate delivery -immunoglobulins and vaccination IM post partum (90% effective) then normal immunization routine @ 2,4,12 months -breast feed is fine other than HIV unless crackled nipples -organize serology at 6-12 month to confirm presence or absence of transmission Mom: -High rx preg > sepcialist involved -regular LFTS needed -matneral antiviral therapy (PEG + Interferon) may be used in 3rd trimester in actively infective moms to reduce transmission Delivery: -no fetal scalp electrode (cilp): during labour > placed on scalp to measure heart rate -avoid instrumental delivery if possible S: screen household contacts: reduce rx of immediate re-infection

Pre-conception

History: start with: 1. Normal medical Hx: Risks PDAFO 2. Disease prevention: vaccination (rubella +chicken pox), folate, listeria 3. Screen head to toe Advanced maternal age >35 years old are a/w: 1. ^ rx of antepartum cxs > pre-eclampsia, gestational diabetes, chronic hypertension 2. ^ rx of pre-term delivery and cesarean section 3. ^ risk of fetal chromosomal abnormlaities that may require additional screening PHx: 1. When was ur last CST? 2. Hx of Gestational Diabetes, T1DM, T2DM? -Aim for HBA1C of <6.5 befor epregnancy to minimise risk of cxs. Drugs: Common contraindications: -anti-hypertensive: ACEi and diuretics r CI -anti-epileptics: need additional folate supplement -any contraceptives should be stopped -allergies should be controlled FHx: -genetic disease -pre-eclmapsia -Gestational Diabetes mellitus -ectopic preg -depression and mental health Vaccinations: BVIM: -boostrix: DTP: pertussis for whooping cough: safe during preg -Varicella: should be done before preg -Influenza: done during preg -MMR: rubella: done before pregnancy: 1 month after Obstetric Hx: -GPA: preg, births, abortions/ectopic/miscarriage -Prenatal Hx: planned or unplanned? -Antenatal Hx: length of gestation, cxs -Perinatal Hx: mode of delivery: cesarean/vaginal/forceps -Post natal: cxs: before, during, after Diet: SAVES Weight: -stop smoking, alcohol, veggies, fruits, stress mx, weight control Folate and NTD's: -0.5mg 3 months before conception and 3 months after -PHx of NTDs or medications (anti-epileptics): MUST KNOW: 5mg 3 months before and 3 months after.

Termination: medical > drugs: mifepristone and misoprostol

How: mifepristone: -anti-progesterone > terminates pregnancy by inhibiting progesterone that maintains endometrium and fetal/placental adhesion -ischemic eff in endometrium causes contractions to remove POC Misoprostol 800ug PO or PV: higher dose than priming the cervix: -prostaglandin F2 Alpha promotes contractility of myometrium and expulsion of POC. Comes undder PBS in a pack togethher: Day 1: Mifepristone 200mg: will get minor period like bleedign and may miscarry before misoprostol Day 3: Misoprostol 800ug: begin to bleed w/in few hours of prostaglandin. Should look for membranous POC. Much heavy, slighly more painful period. Effective: 95% success rate . 5% require surgical intervention Risks: -failure: less effective than surgical intervention -pain: cramping sort of period pains from contraction of uterus: mxed with simple anlagesia Second trimester (rare >14 weeks) -Mifepristone and misoprostol Day 1 and Day 3. Effectiveness reduced with 10% of pts requiring surgical intervetnion. Thus not first line -Risks: risk of failure 10%, risk of severe bleeding. Benefits: private of own home. Easier. Avoid surgery and associated risks

Urinary incontinence types and Hx: BFLQ:

Hx: -how bothersome is it? Any pads? -how freq is it -how long has it been occuring -how much is the leakage? -when does leakage occur? Activity such as Stress: coughing, lifting, exrcise, urge: when they feel they needed to empty bladder but coudnt get there on time, or both -how many births, trauma?, impact on QOL and desire for tx, -constipaitaon, caffeien, OH, smoking, bowel incontinence? Ix: physical ex: abdo, pelvic, perineal -Stress incontinence: cough test if stress incontiencen present -urinalysis: infection -assess pelvic floor muscles -assess PVR: for overflow -Storage Bladder: FUND: freq ,urgency, nocturia, dysuria (pain/burning) -Voiding SHED obstruction: BPH/prolapse: stream, hesitancy, emptying incomplete, dribbling. Stress: -RFs: post menopausal > urogenital atrophy, multiparous, vaginal deliveries/tears, obesity, exercise/lifting -pattern: worse w/ straining -bowel incontiencne: 3rd and 4th degree tears during preg a/w ongoing bowel incontiennce Urge or overactive bladder: day frequency >7 times, Nocturia >1, bed wetting and urgency -idiopathic, PHx: PD, MS, stroke, dementia, -water, OH, caffiene consumption -UTI, diabetes Hx: get urg to go but cant hold it in before reaching toilet -bowel incontinence? (Due to neurological causes: stroke, PD, MS dementia) Overflow: -post menopausal, known pelvic organ prolapse, recurring UTIs -Storage fund, voiding shed -bulge or protrusion? Worse on straining/constipatiotn Stress: coughing, sneezing, laughing, running, lifting -caused by urethral hypermobility where urethra is no longer supported by muscles and ocnnective tissues of levator ani > A. Post menopausal -multiparity -traumatic labour -obesity -heavy lifting Urgency: sudden desire to pass urine difficult to hold > 1. Urgency urinary incontinence UUI or Overactive bladder: Hx: urgency comes > cant make it to toilet on time > detrusor muscle is over active > A. Idiopathic B. Neurological C. UTI D. diabetes E: Diuretics: caffiene, OH, meds Dx: cytometric examination: bladder contracts unpredictablly Mx: anticholinergics oxybutining Mixed: pt have both stress and urgency incontinence Overflow: obstruction to outflow of urine > difficulty completely emptying bladder. -overdistended bladder due to hypotonic bladder -Hx: Loss of urine with valsalva, dribbling, diabetes, spinal injury -Occurs in prolapse, urinary tract malignancy Dx test: Post voidal residual catheterizaitaon PVR Tx: intermittent self catheterization

PCOS: Omg TaSt DHEAS Lips ProPerly.

Hypothalamus: Rapid GnRH pulses > pituitary > elevated LH relative to FSH -LH promotes androgen production via adrenal glands >> ^ androgen production and increased responsiveness to ACTH is enhanced. -High androgens may cause insulin resistence > compensatory hyperinsuliema > causes androgen production -Insulin modulate GnRH secretion. -The abnormal ^ LH and low FSH leads to incomplete follicular development >> polyciytic ovarian morphology Ix: Omg TeSt DHEAs Lips ProPerly (OGTT, testosterone, TSH, DHEA, Lipids, Progesterone, prolactin) Serum total and free testosterone DHEA Serum 17 hydroxyprogesterone and prolactin TSH OGTT Fasting lipid Mx: 1. Counselling: stress inhibits fertility

Endometritiis

Inflammation of endometrium caused by infection -differs from chorioamnionitits bc it occurs after baby has been delivered (post partum endometritis) or following a miscarriage (postabortal endometritis) -generally occurs at the open placental bed. (Site of the placenta) > can spread to local endometrium (parametritis) or more systemically to peritoneum > septic peritonitis or systemically bacterial sepsis. Aetiology: -Group B streptoccous (most common and reason for perinatal ABs) and other normal flora of the vagina (lactobacillus) -STIs: CT or NG -Clostridium perfringins > backyard abortion Rfs: -miscarriage or after childbirth -prolonged labour or cesarean delivery -multiple vaginal exams, hysteroscopy, -retained products -IUD -D&C: uterine scraping Consequences: local/systemic infection > serious maternal conseq. Septic abortion can be fatal Hx: -uterine tenderness -vaginal d/c and odor -fever and tachy -bleeding Ix -high vaginal swab > vaginal flora -fpu > STI -fbe for infection -pelvic ultrasound Mx: -admit, stabilize, call for help -Cover chalmydia > azithromycin -cover gram positive and gram negative aerobes > augmentin -severe is tx same as chorioamnionitis: Gram + > ampicillin Gram - > gentamycin Anerobes > metronidazole

Urinary Incontinence

Involuntary loss of urine. -stress incontinence: inability to maintain continence during strain/compression: cough, straining, weight lifiting, running) -Urge incontinence: inability to hold urine -overflow incontinence -mixed urinary incontinence -Increased intraabdominal pressure forces urethra against intact pubocervical fascia > closing urethra and maintaining continence. -Defective fascial support allows posterior rotation of the urethrovesical junction due to increased pressure, opening urethra and causing urine loss. SNS to promote Storage: -bladder: relaxed > controlled by beta adrenergic recetpros of sympathetics (thoracolumbar > arises from splanchnic nerves > move through hypogastric plexus T10-L2) -internal urethral sphincter: contracted by sympathetics -External urethral sphincter: contracted by pudendal nerve (somatic) > S2,3,4 keeps piss and shit off the floor PNS: promote EmPtying: -Bladder: contracted > parasympathetics: distention > contraction of detrusor smooth muscle Muscarinic 2/3 receptors. PSNS is craniosacral and arise via sacral splanchinc nerves S2,3,4. -internal urethral sphincter > relaxed: parasympathetics -External urethral sphincter: Contracted to relaxed via pudendal nerve (somatic): voluntary relaxation of levator ani muscles via pudendal nerve allows opening of urethra to open and urine to be passed. -Activation of ANS (SNS/PNS) controlled by PONS > Primary micturition center PMC -Epi: 25% of women supper common and is on the rise w/ age Aetiology: 1. Increasing parity (birth) 2. Vaginal delivery 3. Episiotomy All r a/w stress incontinence (coughing, straining, weight lifting, running) -Due to weakening and stretching of muscles during delivery as well as damage to pudendal and pelvic nerves. -burning w/ urination, trouble starting flow, inability to stop flow, needing to push/strain while urinating, needing to urinate more than once to empty bladder, noctria r precursors of urinary incontinence -Dementia may be a/w increased incontinence in older women. -Streneous activity (weight lifting, increases stress on pelvic support structures > eads to stretching and weakening of muscles, nervces and results in urinary incontinence * RFs: -increasing age -increasing parity (births), vaginal delivery, episiotomy r a/w stress incontinence -obesity -lower urinary tract sxms: burning, trouble starting/stoping, needing to push. -dementia -constipation: prolonged straining contribute to neuropathy and dysfunction. -fecal incontinence -weight lifting: increases stress on pelvic support structures -pelvic organ prolapse -stroke: detrusor hyper-reflexia due to upper motor neuron lesion after stroke > urinary urgency/incontinence -parkinsons disease: upper motor neuron lesion > incontiennce -multiple sclerosis: upper motor neuron lesion -diuretic use: cause polyuria, freq, urgency -caffiene: freq and urgency Hx: -rfs -urine leakage on effort, exertioin, sneezing, coughing: suggestive of incontinence -urinary leakage preceded by urgency -freq urination -bladder diary: 3 day >records each void and fluid intake -vaginal bulge/pressure -urogenital atrophy: thin poory vascularised urogenital tissue -Hx of stroke, parkinsons -back injury -dysuria: suggestive of UTI -urethral d/c or tenderness: suggest urethral diverticulum, carcinoma, inflammation DDX: -urogenital infections: bacterial cystitis, prostatitis, urethritis -Endometriosis -bladder cancer/calculus, interstitial cystitis -psychogenic urinary freq -constipation Reversible causes of incontinence in elderly: Diappers: -Delirium -infection -atrophic vaginitis -pharmaceuticslals -psychological -excess fluid -restricted mobility -stool constipation Ix: -urinalysis: UTI may cause urinary urgency, freq and urge/incontinence -empty supine stress test: + if urine leakage -post void residual measurement (PVR): confirms urinary retention -cough stress test Mx: Stress incontinence: -weight loss, reduce caffieen/OH intake, aim <2L of water per day, stop smoking -correct menopausal vaginal changes -pelvic floor rehabilitation -vaginal/urethral devices: pessaries Urge incontinence: -bladder retraining -pelvic floor rehab -tx constipation, weight loss, reduce caffeiene/OH -Anticholinergics > PNS>Relaxes contractions of bladder > Anticholinergics (oxybutinin): ANTI SLUD: saliv, lacrim, urin,defec -Merabegron > SNS> beta 3 adrenoreceptor agonists: increases storage capacity -Peripheral nerve stimulation -Surgery : intravesical botox or sacral nerve stimulator or augmentaitaon cystoplasty Medication review: stop any diuretics, antidepressants Diabetic educator: re-assess glycemic control Reduce caffiene intake Tx UTIs

Women infertility Ix

Ix: 1. Semen analysis and antisperm antibody for male partner ***ALWAYS 2. Endocervical swab or first pass urine Nucleic Acid aplication Test for chlamydia and gonorrhea and urinary B-HCG test 3. Luteal phase progesterone: assessed 7 days after ovulation (day 21). >9.5nanomol/L > means ovulation. <31.8 nanomol/L is a/w infertility. 4. urinary LH: ovulation can be detected with urinary LH prediction kits 5. Anti-Mullerian Hormone suppresses other follicles in ovary during follicular phase. Correlates with FSH levels . 6. TSH levels 7. Transvaginal ultrasound scan: asses pelvic organs + ovaries. Can be polycystic, abnormal uterine structure, fibroids, endometrial polyps, hydrosalpines. 8. Hysterosalpingogram (X ray of uterus and fallopian tubes): done at day 7-11 before ovulation and after period. -hydrosalpinx: tube is blocked > causes build up of fluid near the ovary > sausage shape on scan. 9. Hysteroscopy 10. Karyotyping: may show chromosomal abnormality > turners syndrome. Serum prolactin, estrodiol, FSH/LH, free testosterone-elevated in PCOS (if ovulation is not confirmed with initial tests) -Serum LH and FSH is performed in amenorrhea.

Infections in pregnancy

Key infections of anatomical structures : 1. Uterus: chroioamnionitis, endometritis 2. Urinary tract: UTI and pyelonephritis Infections screened for or actively advised about antenatally: 1. Hepatitis B and C 2. HIV 3. Rubella 4. Syphilis 5. Varicella Zoster 6. Listeria 7. Group B streptococcus

Labour pain and analgesia

Labour pain: 1. Early 1st stage: -distension of lower uterus and endocervix as baby begins to descend into pelvis -sympathetics T10 > L1 -Pain is poorly localized bc its viscera origin thus refered to dermatomes T10 and L1 >> pain across lower abdo and upper thighs. 2. Late 1st stage and 2nd stage: -Pain in vaginal walls and perineum -Pudendal nerves S2 > S4 -get pressure deep in pelvis + intense burning feeling in the perineum. Nonpharmacological: Supported: 1. Social support: may be father, partner, friend: women w/ social support requires less analgesia during labor 2. Relaxation techniques: deep breathing exercises, yoga, preparation (birth plan) and education 3. Warm water: can be effective for pain 4. Hypnotherapy: mots supported alternative analgesia reducing neuraxial in upto 25% of women. Eg. 6 1 hour training session in 3Tri. Less evidence 4. TENS machine: controls pain of labour but theres no evidence 5. Aromatherapy Pharmacological: on labour ward: 1. Inhaled nitric oxide: moderate analgesia in 50% of women. 2. IM Pethadine (opioid) 3. Epidural: sensory block, minimal motor block 4. Other: sterile water injections, PR Diclofenac In theater: A. pudendal nerve block: anesthesize the perineum. Pudendal nerve leaves lumbosacral plexus into posterior compartment of thigh via the greater sciatic foramen below the piriformis > then passes back into pelvis through lesser sciatic foramen. Local anesthetic inejcted at ischial spine to anesthetize the pudendal nerve. B. spinal anesthetic: * given in subarrachnoid space -predominately used in elective CS. Need is larger and inserted through Ligamentum flavum and in through the dura mater (2 pops) -performed at level of L4 (iliac crest) and L5 (PSIS): below the conus medullaris in teh cauda equina -anesthet of nerves of cauda equina > paralysis from level below > no movement of legs and contractions r NOT felt. *sensory block and motor block C. general anesthetic -used in emergency CS where u immediately need to get baby out. Rxs: -mom: allergic rxn, N/V, damage to teeth from intubation -neonate: resp depression

Obstetrics History: need to include:

Last pregnancy: -GPA: pregnancies, births, abortions/ectopics/miscarriages -cx's This pregnancy: -Planned, normal or IVF -Preparation: folate and rubella checks? -Gestation? -care upto now -sxms now: screen according to gestation: pain, bleeding, NV etc If in labour: -antenatal Hx: scans, problems and major medical conditions -What stage? -maternal well being-vitals, analgesia -membranes: intact and color of liquor -fetal wellbeing: HR or CTG: 110-160

Listeria:

Listeria monocytogenes > gram + baccili and anerobic -listeris is ubiquitous (found everywhere) -affects ppl w/ immuno sup : young, elderly, preg -most common 3rd trimester Avoid: non pasturized dairy, milk, soft cheese, raw seafood, meats Maternal Infection: -flue like illness + myalgia + lethargy -fetal distress > meconium staining of liquor often seen <34 weeks as lighter brown vaginal discharge -major rx to mum and bub > prematur labor Identified w/ high vaginal swab + culture and blood cultures Fetal cxs: -fetal death in utero or severe morbidity may result in vertical transmisison (travels easily across placenta) NIRS R: ABx: IV Ampicillin + Gentamycin

Multiple pregnancy Mx and dates for antenatal care of twins

Preconception: 1. High dose 5mg folate supplementation 2. Fe supplementation 3. Low dose aspirin to prevent pre eclampsia + regular BP checks First trimester screening: -normal first trimester Dating ultrasound + nuchal translucency scan. 18-22w > normal morphology US 24-26w > OGTT for GDM Serial monthly biometry every 2 weeks from start of second trimester 32 weeks > weekly CTG. Delivery: When: -dichorionic > 39 w -monochorionic > 37 w How: depends on leading twin > must be cephalic. Second twin can be cephalic, breech or transverse and vaginal delivery is still possible w/o cesarean *Delivery of second twin in transverse position > better to deliver breech > from the legs *reason we dont deliver the first twin if its breech is bc if the 2nd twin is cephalic > the necks of the babies can lock in the pelvis>> cause fetal death in the leading baby and warrant amputation at the neck to allow delivery of second twin.

UTI and Pyelonephritis

Lower UTI: infection and inflam of urethra (urethritis) and bladder (cystitis) Upper UTI (Pyelonephritis): ascending infection present in the ureters and kidney. Bacteremia occurs in 20% of pts and severe sepsis represnts a small portion of this. Why in pregnancy? -Urine: during preg > ^ glucose and protein is present in the urine plus a less acidic pH > easier for bacterial colinization -Progesterone: maintians smooth muscle relaxation > dilates ureters making hydronephrosis and reflux more likely. This ^s rx of pyelo -asymptomatic bacteuria: 6% of bacterial infec that is asymptomatic. 2% of pregnancies will develop bacterial pyelonephritis if untreated ths all women get MSU on conception -coliforms: normal flora of gut and genitourinary tract: Anerobes > E. Coli Gram positive > staph saprophyticus Gram neg: klebsiella, proteius, enteroccus hx: move up urinary tract: -urethra: buurning stinging, smell? -bladder: storage FUND -kidney: flank pain, N/V, F/R/N -vitals: febrile > sugests pyelonephritis or sepsis -tender bladder: a/w cystitis -flank tenderness: > pyelonephritis Ix: -MSU: dipstick + MCS -FBe -UEC -renal ultrasound: in suspected cases of pyelonephritis ot look for signs of hydronephrosis -Pyelonephritis: loin pain and tenderness on palpation of kidny, fever -Cystitis: urinary freq, nocturia, suprapubic pain, hematuria -urethrtis: burning or stinging, smelly urine. Mx: -UTI: amoxicillin/clavulonic acid, cephalexiin or NITROFURANTOIN r used -pyelonephritis: ampicillin +gentamycin OR just give ceftriaxone A. A proof of cure: msu is required and the pt is started on prophylactic nitrofurantoin for the remainder of the pregnancy. ****In the non pregnant lady > trimethoprim is used as first line for UTIs and Ciprofloxacin is 1st line for pyelonephritis. But is CI in preg > teratogenic. Non pregnant: UTI: trimethoprim Pyelonephritiis: ciprofloxacin

Risk of intrumental delivery

Maternal: -PPH: tone, trauma, tissue, thrombin -genital tract trauma Fetal: -scull fracture and IC hemorrhage: -chignon: welling w/in soft tissues of scalp > disappears w/in first 24 hours and common w/ ventous -subgaleal hemorrhage: rupture of small vessels in scalp: above periosteum -cephalhematoma: below periosteum. Does not cross midline or suture lines. Resolves w/in weeks. Generally uncomplicated

Antepartum hemorrhage emergency management

Mom: DRS ABC + Resuscitation 1. Paper work: commence fluids and estimate blood loss 2. IV access: send for FBE, Coags, cross match + KB test and give anti D 625 IU. 3. Baby: CTG While this is happening, im going to assess the cause of APH Mom: Hx ,Ex, Ix -review hx and scans -do speculum examination: if there is obvious visible source of bleeding like the cervix -get USS transvaginal US ASAP: looking for Placenta Previa or abruption +/- compliation with accreta (accreta may need MRI to confirm but lady is unstable there is no choice) Treatment: -Fetal death > vaginal delivery -maternal/fetal compromise > immediate C/S -No compromise: -<37 weeks: manage as PTL (STATIN: prevents myometrial contraction, cervical remodeling and preterm labour) or close follow up - >37 weeks: elective (planned) cesarean section Cesarean section consent: IPBRAAD: -Indication: cesarean section is needed to be done due to the safety of you and your child: in your case, due to blood loss -Procedure: Before: will recieve anesthetic which will numb you: risk of damage to nerves, infection but chances r low During: will deliver your baby with curtain up so you cant see anything. You will be awake and monitored the whole time After: you will have to stay in the hospital for a few days and healing can take upto 6 weeks. -Benefits: everything will be well monitored for your safety and your babies safety, preventing blood loss -Risks: bleeding, infection, damage to surrounding organs, pain, impact on future pregnancies, sedentary (risk of clots), anesthetic risk, and risk of hysterectomy if there is a cx like placenta accreta or major bleeding that wont stop. *standard obstetric emergency care: 1. Call for help 2. Document and debrief w/ family 3. monitor for prenatal depression.

Women's Health History: gynae or obstetrics

Name Demo HOPC: SOCRATES PDR Site: where is pain Onset: when did it start Character: is it sharp or dul Radiation Associated sxms Timing: does pain vary in intensitiy during the day Exacerbating/alleviating: anything make it worse/better? Severity: does it interfere with daily acitivities? Periodicity: how often does it occur Duration: how long does pain last Reoccurence: have u had this pain before? Menstrual Hx: 1. Menarche/menopause start 2. LMP: last day of period? 3. Length of bleeding? 3-7 days is normal 4. Frequency: how often do u get ur periods 5. Regularity: bleed 3-7 days, cycle 21-35 day cycle. >35 irregular 6. Bleed between periods? (IMB: intermenstrual bleeding) 7. Post coital bleeding? 8. Post menopausal bleeding? Heavy? Clots? Flooding (stain bed sheets)? Past gynae Hx: 1. Gynae sxms: bleeding between periods, ^ urination/burning, pressure, itch/swelling of vag, lumps or discharge, odor? 2. Gynae Dx's 3 Gynae surgery 4. CST: date and results 5. Contraception: methods of protection against pregnancy? Past Obstetrics: 1. GPA: number of preg, number of births, number of abortions, miscarriages, and ectopics 2. Dates of delivery 3. Length of preg 4. Spontaenous/induced/instrumental 5. Vaginal/cesarean 6. Sex and weight of baby 7. Cxs before, during or after pregnancy PMHx: 1. Medical illnesses 2. Hospitalizations/surgeries Drug Hx: 1. Medications 2. Herbals 3. Recreational drugs 4. Allergies Personal Hx: SADAM Wajid husain -sleep -appetitie -defection -addiction -micturation -weight changes FHx: 1. Medical/gynecological conditions 2. Malignancies 3. Consanguinity (cousins) Social Hx: 1. Occupation 2. Support network 3. Smoke/OH 4. Marital status

Pregnany symptoms: early signs

Nausea and vomitting Breast tenderness Amenorrhea Ankle swelling HCG levels >5 pregnant 10 weeks: highest peak: 25,000- 250,000 then declines by 16 weeks then stays at a steady state. -Since highest levels of HCG is between 5-16 weeks, this defines the window for majority of hyperemesis gravidarum. *******Normal pregnancy: B HCG doubles every 2 days until it reaches 10,000 to 20,000 -Ectopic: b HCG levels increases less.

Management of common sickness

Nausea and vomitting: -seen in 50% of preg a/w rising BHCG levels: protective mechanism telling u to eat. Subsides after first trimester Mx: -reassurance -conservative therapy: small freq meals, ginger, fizzy drinks, and avoid cooking environemtns or strong smells, regular hydration. GORD: -small reg meals -avoid spicy or acidic foods -upright after meals -reduce smoking and caffiene -meds: antacids such as mylanta, PPI such as esomeprazole or H2 receptor antagonist (ranitidine) when severe Cramps: magnesium helps Varicose veins: can be embarrassing and mxed best with elastic stockings or tights to support the veins and reduce social anxiety Constipation: -caused by presence of progesterone > decreases action of smooth muscle (prevents uterine contractions as well) -^ water intake, fiber, exercise, laxatives (lactulose) Hemorrhoids: -prevent it with ^ fiber. -painful hemorrhoids: local anesthetic ointments or saline gauze packs -dental hygiene: ^ risk of gingivitis and epilus (granuloma formation of gums a/w bleeding but is benign) during pregnancy -back pain: common in lumbar/thoracic spine Mx: lifting and twisting techniques, avoid high heels, sleep on hard mattress, physio Carpal tunnel: -reassurance -brace to reduce load -educate on overuse -corticosteroid injections if it persists Hypotension: -dizzy spells esp postural is common ft due to venous return from legs and head. -when sleeping/lying > lay on left side to avoid compressing inferior vena cava. IVC sits on right. Pruritus: -a/w cholestasis given ^ estrogen sensitivity -order LFT to assess GGT and ALP -Moisturize skin -abnormal LFT > further IX and imaginign of gall bladder

Preterm labour complications

Neontal morbidity and mortality: -<26w: neurological damage occurs in 1 in 4 babies resulting in morbidities such as A. Cerebral palsy B. Blindness C. Deafness. D. Retinopathy of prematurity (related to O2 therapy to tx respiratory distress) E. ^ed rate of behavioral problesm and ADHD *Cervical ripening (dilation/effacement/softening) > this is preterm labour and needs immediate mx *non ripening: this is threatened preterm labour: contractions w/o cervical changes ***Water can break even before contractions begin >> this is Premature Rupture of Membranes PROM. If <37 weeks this is PPROM > preterm premature rupture of membranes.

Secondary amenorrhea

Normal period: -menses: 3-7 days -follicular phase 7-21 days: ovulation occurs at the end -Luteal phase: fixed duration always 14 days Normal bleeding occurs for 3-7 days, and cycles are between 21-35 days. Amenorrhea: -primary: failure of menses to occure before age of 16 or 2 years after onset of puberty. -secondary: cessation of menses after it begun. Cessation must be: A. >3 months in a women w/ regular cycles B >6 months in a women w/ irregular cycles. K= menses (3-7 days)/ cycle length (21-35 days) DDX: 1. Hypogonadotropic: (at hypothalamus) > low FSH and LH: -High or low BMI -Diet restriction, heavy exercise, stress -sheehans syndrome (past complicated labor: post partum hemorrhage)? -prolactinoma/pituitary adenoma: High prolactin inhibits GnRH (thus low FSH/LH): Prolactin produces milk during preg and inhibits ovulation to prevent preg while breast feeding. 2. Eugonadotropic > ovarian dysfunction -PCOS: insulin resistance thus high insulin, low FSH and high LH A. Hx: infertility, hirsuitism, acne, overweight, loss of hair on scalp B. Ix: ^ total and free testosterone, DHEA (dehydroxyepiandrosterone), and 17 hydroxy progesterone, serum prolactin, OGTT, fasting lipid C. Mx: counselling, SAVES WEIGHT, metformin, clomid. 3. Hypergonadotrophic > ovarian failure. -Normal or familial early menopause -pregnancy missed 1-3 periods. Number 1 cause of amenorrhea => Q's: sexually active? Contraceptive? N/V, breast tenderness, swelling -Physical obstruction: uterine synechia or trauma to cervix > result in adhesions. => cyclic pain but no bleeding? -Iatrogenic: surgical intervention for miscarriage => surgical procedures? curtagge or ablation? -breast feeding: women worry why they dont get their period post natally but they r breast feeding still. Prolactin inhibits GnRH (low FSH/LH) thus no ovulation and amenorrhea. -Thyroid: A. Hyperthyroidism > periods r light/absent => Weight loss, heat intolerant, tremor B. Hypothyroidism > amenorrhea. => weight gain, cold intolerance, tired/weak -Cushing's: A. High cortisol due to pituitary tumor (cushings disease) B. Cushings syndrome > adrenal gland/GCC> hypercortisolism => weight gain, acne, hirsutism. Taking GCC?

Diagnosis of IUGR and management

Normal screening for fetal growth (20 weeks): -Fundal height + fetal biometry (estimated fetal weight) Can be either normal or if SGA (<10th centile) then do: 1. Fetal biometry (assess AC/BPD for symmetrical growth restriction > decreased abdo circum and head size BPD 2. AFI: amniotic fluid index: decreased perfusion to kidneys > low AFI 3. Umbilical and MCA doppler > reduced, absent or reverse umbilical doppler and ^ed MCA doppler (head sparing) 4. Biphysical profile (breathing,movement,tone, AFI,CTG) : 7 or less is IUGR baby 5. Kick chart: new fetal movements are decreased **Repeat after 2 weeks to assess tracjectory Diagnose IUGR baby Mx: -specialist: have ^ed maternal and fetal rx thus need to refer to specialist: pediatric services and neonatal ICU/nursery -Delivery requirement: vaginal +/- cesarean section: -Induction of labor at <37 weeks in confirmed IUGR has lower maternal and fetal problems -IUGR baby is less able to tolerate contractions compared to normal term baby thus mechanical balloon catheter induction of labour is used to eliiminate the risk.

Number of contractions, dilation, and time of labour

Number of contractions: stage 1 latent phase: 1-3 contractions/10 mins, stage 1 active stage: 4-5/10 mins. >6 /10 min is tachy *Prolonged first stage (latent stage): primi >1cm/hr, multi >1.5 cm/hr * prolonged second stage: primi > 2 hours, multi >1 hour +1 for epidural. Furhter failure to progress >> obstruction > need cesarean section

Management of common questions 1st and second trimester

Nutrition: -fiber: minimise risk of constipation caused by progesterone -folic acid: 1 month before 3 months after conception (SHAVI confirmed this) -milk and dairy avoiding unpasturized products (listeria) -multivitamins Smoking/OH, caffiene, drugs: -stop smoking + passive smoke -stop OH > FASD is leading cause of mental impairment -no safe lower limit -caffiene: max 1 cup of coffee -drugs: no Breast feeding: recommend breast feeding unless you have HIV or Hepatitis C. Antenatal classes: give access to services to provide education, ad support Normal activities: normal work and activities should be continued as long as possible. Most stop work a month before due date Sex: continue but avoid in placenta previa. Travel: -Air travel is ok until 36 weeks. More than 36 weeks is not recommended and may need medical clearance in women >36 weeks -continue wearing seatbelt despite discomfort. -weight gain: 10-15 kg weight gain mostly after 20weeks > due to baby growing and body preparign for milk production -fetal movement: Most women report fetal movements by 20 weeks gestation A. Primigravida: 18-20 weeks B. Multigravida: 15-17 weeks Rubella exposure: assess rubella serology. 3rd trimester: -non medically indicated induction of labour or elective cesarean at 37-39 weeks is not encouraged due to high rates of neonatal morbidity.

Pre-Mentrual syndrome (PMS) and Premenstrual Dystrophic Disorder (PMDD)

Spectrum of Pre Menstrual Syndromes: A. Nothing B. Pre-Menstrual Symptoms C. Pre-Menstrual Syndrome: fxnal impairment due to physical sxms: abdo bloating(common), breast tenderness, headache, mood changes. D. Pre-Menstrual Dystrophic Disorder Pre-menstrual symptoms: no impact on QOL -80% of women get symptoms Pre-menstrual syndrome (PMS): impact on QOL -1/4th of women -Cyclic recurrence of sxms that occur in luteal phase and cause signif impairement on daily life and cease after onset of period -Mood swings, tender breasts, food cravings, fatigue: affects daily activities Pre menstrual dystrophic disorder: PMDD: <5% Sxms still persist post menses. -More severe form and is classified as a mental illness. -Psychological sxms make up majority of dx: DSM 5: 5/11 sxms over a year: = depression/anxiety,irritable, labile mood, loss of interest, concentration, fatigue, appetite, insomnia, physicall sxms ( breast tenderness, headache, ache, bloating, weight gain) PLUS impact on social/work -AKA pre menstrual exaggeration of underlying illness Epi: PMS: 20% of reproductive age PMDD: 8% Aetiology: PMS/PMDD dont occur before puberty or after menopause. -due to role of steroid hormones. -Dietary factors and vitamin def -Genetic component -mental illness (Obsessive compulsive personality disorder) Pathophys: -interaction of changing hormonal levels with serotonin, beta endorphin, GABA and autonomic nervous system. -Serotonin drugs SSRIs such as fluoxetine relieves PMS/PMDD sxms. RF's: 1. FHx 2. Mood disorders 3. Smoking Hx: -rfs -bloating -fatigue -breast tenderness -headache -depressed mood, irritability -labile mood Ix: -sxm diary -TFT -FSH Dx: 1. Occur over consecutive cycles 2. Atleast w/in 1 week of menses 3. Resolve or remit w/ period Mx: 1. Keep a diary to track sxms 2. Explain and reassurance 3. Refer to psychologist > CBT 4. SAVES weight Mild sxms 5. Calcium and B6 vitamin 6. Second line: COCP Severe PMS/PMDD: 7. SSRI: fluoxetine -saves weight -CBT -NSAID -calcium and vitamin B6 supplementation -2nd line: COCP -3rd line: GnRH agonist: if SSRI and COCP r unsuccessful -4th line: surgical oophorectomy

Post partum hemorrhage:

PPH > Blood loss after delivery: -Vaginal delivery > 500 ml -Cesearean section > 750 ml -Severe PPH is blood loss >1000ml. Primary PPH: within 24 hours of delivery Secondary PPH: btwn 24 hours - 6 weeks Epi: 4% with active 3rd stage Mx (oxytocic injection) 8% w/ physiological 3rd stage mx (natural) 10% of all maternal mortality RFs: -multiple pregnancy > tone -previous PPH > tone -Preeclampsia > thrombin -macrosomia > tone -failure to progress in second stage > tone -Prolonged 3rd stage > tone -Retained placenta > tisue -placenta accreta > tissue -episiotomy > trauma -perineal laceration > trauma -general anesthetic > tone Aetiology: 4 T's: second letter in reverse alphebetical order Tone: 70%: -over distended uterus: limits ability to contract after delivery >>thus any factor that causes prolonged stretching of the muscles will ^ rx of PPH >> RFs: polyhydramnios, multiple pregnancy, macrosomia -uterine exhaustion: over exerted thus poor arterial ligation >>RFs >> prolonged labour, oxytocin IOL, rapid labour -Intra-amniotic infection: stimulate inflammatory response > limit myometrium contrraction after delivery >> RFs > prolonged ROMs. -Drug induced hypotonia of myometrium: A. Physiological mx: dont give oxytocis > muscle works hard >> Atonia B. Magnesium sulfate > in women w/ PET for neurological preevntion oro in women w/ preterm labour <30w C. Nifedipine: peripherally acting CCB reducing smooth muscle contractility D. Salbutamol: B2 agonist: promoting smooth muscle dilation/relaxation Rfs: physiologicalc mx of 3rd stage, MgSo4 (PET), Nifedipine (HTN), salbutamol (asthma) Trauma (20%) : and its RFs -episiotomy/ perineal tears >> IOL, instrumental delivery -surgical incisions: CS -uterine rupture: VBAC -Uterine inversion: fundus of uterus collapses in on uterine cavity or prolapse through vaginal cavity thus placenta fails to detach Fts: no uterus palpable on abdomen, large mass over cervix, shock. Mx: manual relocation of uterus RFs: strong contractions in 3rd stage, short umbilical cord, high parity, uterine relaxation Tissue (10%): -Retained placental products: retention of placental tissue (cotyledon) prevents occlusion of placental sinuses. >> abnormal placental US (bilobed placenta or accreta, high parity, previuos CS) -placenta accreta: percreta (placenta protrudes through uterine wall and involve local structures > bladder): fts: PHx CS, low lying anterior placenta, Raised AFP. Mx: emergency surgical removal or hysterectomy Rfs: PHx of CS, US low lying anterior placenta Thrombin (<1%): abnormalities of coagulation: -thrombocytopenia -PET -ITP -Factor disorders -VWD -Hemophilia -DIC -severe infection

Preterm rupture of membranes PROM VS PPROM Mx

PPROM: STATIN -steroids dexamethasone -transfer to tertiary care -abx: erythromycin and ampicillin -Benpen or clindamycin for GBS prophylaxis -Chorioamnionitis: AMG: ampicillin, metronidizole, gentamycin T: tocolytics: nifedipine CCB I: intrapartum monitoring of mom and fetus + obstetric + pediatrician N: neuroprotectant: magnesium sulfate PROM: 1. Expectant with risks explained: have 96 hours (4 days) for labour to occur naturally before we induce 2. Term induction of labour: Bishops +/- cervical ripening - 8 or greater: do induction of labour > synotocinon - <8 > must ripen the cervix > prostaglandins or foley balloon catheter 3. During labour: -IV benpen or clindamycin for GBS prophylaxis, continuous CTG monitoring, Obsetric and peds doctor

Pre-eclampsia:

PRE: proteinuria >300mg/24 hrs + Protein: Cr > .3mg/dL, Raised BP >140/90 after 20w gestation, edema Rx factors: MAD High BP Hypertensive syndrome occurs after 20 weeks gestation consisting of new onset, persistnet HTN defined as BP of >/= 140 systolic and or >/= 90 diastolic based on atleast 2 measurements taken atleast 4 hours apart with one or more of: 1. Proteinuria (urinary excretion of >300mg/24 hrs, Protein: Cr ratio >.3mg/dL or 0.03g/mmol 2. Evidence of systemic involvement: A. Renal insufficiency: elevated creatinine: proteinuria> reduction in colloid osmotic p in blood > puffy legs and SOB a/w pulm edema B. Liver involvement: elevated transaminases and/or RUQ pain: in HELLP syndrome (severe pre-eclampsia) C. Neurological cxs: seziures, headaches, visual, stroke D. Hematological cxs 3. Fetal growth restriction EPI: 2-8%% of all pregnancies world wide: 1 maternal death caused by PE every 12 mins Aetiology: failure of normal invasion of trophoblast cells leading to maladaptation of maternal spiral arterioles and is a/w hyperplacentation disorders such as diabetes, hydatidiform mole and multiple preg Pathophys: -failure of normal invasion of trophoblast cells >maladaptation of maternal spiral arterioles > leading to placental insufficiency and thus > >fetal growth restriction -systemic maternal response >>vasoconstriction and capillary leaking >>HTN and cxs such as: 1. Cerebral vascular dysregulation and edema 2. Liver vascular dysreg and edema 3. puplmonary edema *though pre-eclmapsia doesnt occur until AFTER 20 w > the abnormal changes occur from early in first trimester via biomarkers: -pregnancy associated plasma protein A PAPP A -ADAM12 -Placental growth factor -soluble endoglin -soluble fms-like tyrosine kinase 1 Classification: -mild to moderate: BP >140/90 (>140 and or >90) and proteinuria >300 mg /24 hours or Protein: CR >.3mg/dL -severe: BP >160 and or >110 on 2 occuations 6 hrs apart + proteinuria >300mg/24 hrs or Pro:Cr >.3mg/dL -HELLP: severe form of pre-eclampsia characterised by Hemolysis, eleveated Liver enzyme, low platelets. (Mild: >140/90, moderate >150/100, Severe >160/110) Rfs: MAD High BP: multigestation, age ^, diabetes (gestational), HTN, BMI>30, PCOS -primiparity: given birth to only 1 child. Strongly a/w primiparity. 2x as high vs multiparous women -PHx and FHx of pre-eclampsia in prev preg -BMI >30 -maternal age >35 yrs -twin pregnancy -subfertility -gestational HTN: HTN >20 weeks gest in absence of both proteinuria and systemic sxms) go on to develop PE -Gestational diabetes -PCOS: due to ^ed rx of obestity, T2DM and tx for sub-fertility -autoimmune disease: antiphospholipid syndrome: anticardiolipin, lupus coagulant -renal disease: may already have HTN and proteinuria -chronic HTN Hx: Go from head to toe: neuro: frontal headache, visual changes, dizzy. Heme: anemia: from hemolysis > tired, cold, pale. Renal: a/w endotheliosis in glomerulus and loss of protein in urine > odema and SOB. Liver: N/V, RUQ or epigastric pain, itch. Obstretic: fetal movements? ->20 w gestation -BP >140 and or >90 in a previously normotensive women is dx. Measure 2 times, 4 hours apart. Severe if: >160/110 (high systolic BP is a/w stroke and placental abruption) -headache (frontal headache) -RUQ pain: occurs in 16% of pts of severe disease and is clinical sxm of HELLP syndrome (subtype of severe pre-eclampsia characterised by hemolysis, elevated liver enzymes, low platelet). -reduced fetal movement -fetal growth restriction: if uterus is small for dates, this implies amniotic fluid volume is reduced > signifies fetal growth restriction. -edema: very common but not used in dx. -visual disturbances: photopsia: flashing lights, scotomata -seizures: indicates ECLAMPSIA and mandates admission to ICU, stabilization and delivery! -SOB a/w pulmonary edema. If pulmonary edema occurs after delivery > it is one of main causes of maternal mortality > this sxm means pre-eclampsia is severe -oliguria: <500ml urine/day or 30ml urine in 2 consecutive hours. May be a/w increasing edema. -hyperreflexia and or clonus *ECLAMPSIA: generalized seizure: -clin fts: hyperreflexia and clonus, frontal headache, blurred vision/photophobia, altered mental state. -lead to stroke Cxs: -IUGR bc of placental insufficiency -Placental abruption -eclampsia -pulmonary edema: largely a post partum event indicated by SOB -preg associated stroke -still birth Ix: -urinalysis: >300mg/24 hrs or urine proteitn:Cr ratio >.3mg/dL -fetal ultrasound: size of baby and amniotic fluid volume -fetal biometry: to dx or exclude IUGR -umbilical artery doppler -FBE: low platelet (HELLP) -LFT: sign of HELLP -Serum Creatinine: UEC -coagulation screen Risk scoring for pre-eclampsia: u are high risk of PReeclampsia if u have any of the high risk or 2 or more of the moderate rfs High risk factors: 1. PHx of preeclampsia 2. Chronic renal disease 3. chronic HTN 4. DMellitius 5. SLE or APS Moderate rfs 1. First preg age >35 BMI >30 inter preg interval >10 yrs FHx of Pre eclampsia Mx: -mild: BP >140/90 > home or day assessment centre -Moderate to severe > admit to hospital -Severe pre-eclampsia >160/110: Labetalol, Nifedipine, Hydralazine, methyldopa ->37 weeks pregnant w/ severe or non severe preeclampsia > induce labour Prevention: Low dose Aspirin to high risk females: reduces development of pre-eclampsia in women w/ ^ rx factors. Delays onset of PE. If u get PE at 26 w > now u will get it at 31 weeks. (5 week delay) -aspirin 150mg at bedtime: start it at first trimester screening (11+5 weeks) *PE and UGR are the same thing nuntil proven otherwise > both are caused by placenta> -Sepcialist involvement -HTN: BP >160 and or >110 1. Labetalol: BB promote vasodilation and SNS drive. SE: bradycardia, bronchospasm, Nausea, scalp tingling 2. Nifedipine 3. Hydralazine Eclampsia: generalised seizure that occurs in preg women w/ Severe HTN -triad: headache, epigastric pain, visual disturbance + hyperreflexia -drug of choice to prevent eclampsia (seizures) is magnesium sulphate Magnesium sulphate: -halves rx of eclampsia -reduce maternal mortality A. 4x ^ in hypotention -MG204 is drug of choice for eclampsia and given as a seizure prophylaxis in severe pre-eclampsia. Give this if the 3 drugs doesnt help > labetalol, nifedipine, hydralezine, methyldopa and if pt has neurological sxms: headache, visual disturbance, dizzy, hyperreflexus/clonus) *Methyl DOPA: centrally acting antihypertensive >reduces sympathetic tone >vasodilation >>^ rx of DVT and Depression > DONT give it in depressed people -BB can cause hypoglycemia in baby. *ACE i and ARBs r CI in preg > a/w fetal death and neonatal renal failure Delivery: -cesarean is common but NVD is an option -STATIN Pre- term mx:

Preterm pathophys and Ix

Pathophys: -for preterm delivery to occur need dilation and effacement of cervix. Hypertrophied fundal pole begins contractions to expel baby -lower segment stretches > ^'s prostaglandins and inflammatory mediators. -cervical change occurs via inflammatory cells -Increased contractility of upper segment is a/w ^ Prostaglandins and oxytocin receptors and gap junctions -infection also causes inflammation and rupture of membranes. Classification: -preterm: 34-37w -very preterm: 28-33+6 w -extremely preterm: <28 w. Ix: -Cardio(fetal HR) toco (uterine contractions) graphy (recording): CTG: >1 contraction every 10 mins -transvaginal US: cervical length <2cm -AmniSure ROM test: diagnostic test to detect PROM: vaginal swab. -cervicovaginal swab for fibronectin > positive: fetal fibronectin concentration correlates with risk of preterm: >200ng/ML >>45% chance of delivering in 2 weeks. -FBE: Antenatal hemorrhage, WCC >infection -CRP > infection -Urine dipstick and MCS> infection -high vaginal/rectal swab > GBS *Fibronectin is a glycoprotein involved in adherence of chorion to endometrial decidual cells: raised fFN suggests delivery is imminent within 7 days (Positive predictive value is 30%) PPV: probability of subjects with a positive screening test that truly have the disease. *From 20-35 weeks fibronectin levels arent high bc the chorion is attached to endometrium. If there is elevated levels >>preterm labour *PPROM is a clinical diagnosis, made on hx sugestive of leaking liquor and confirmed by a sterile speculum examination revealing a pool of fluid in teh posterior fornix.

Antepartum Hemorrhage

Perivaginal bleeding >20 weeks gestation -defined as vaginal bleed >20 ml after 20 weeks gestation until delivery of baby. -APH: majority involves diagnosing 3 conditions: 1. Placenta praevia 2. Placental abruption 3. Vasa Praevia Epi: 3% -bleeding causes irritation of uterus > big cause of pre-term labour and preterm birth > a/w 20% of very pre-term birth -Pre Term labour PTL is major mediator of maternal and neonatal morbidity namely RDS, fetal prematurity and chorioamnionitis. Aetiology: -Placenta: 1. Placenta Praevia: 30% 2. Placenta Abruption: 20% 3. Placenta Accreta 4. Vasa Praevia 5. Marginal bleed/other: 50% -Uterine: 1. Uterine rupture -Lower tract: 1. Cervical bleeding

Non hormonal: Condoms

Physical barrier to passage of sperm into vagina. -New one must be used each time -can prevent HIV and other STDs -Male condoms can also help prevent early ejaculation Failure rate 15%. Benefits 1. Only one to prevent STI Cons 1. Loss of sensaiton during intercourse 2. Lower contraception prevention than others 3. Latex allergy 4. May slip/break

Partogram:

Plotted on partograph begins in active stage of phase 1: LATPA: LA: stage 1: latent 0-4cm, Active: 4-10cm (start partogram here) Transition: mood changes, irrational, pain meds Stage 2: 10cm: Passive stage, active stage (active pushing) Stage 1: Active phase: -every 30 mins: contractions, fetal and maternal HR, liquor -every 4 hours: maternal obs, vaginal exam VE: to assess cervical dilation and effacement and position of presenting part. Stage 2: -hourly: maternal obs, VE: cervical dilitation and effacement and psoition. FHR: every 30 mins Liquor: amniotic fluid is observed and recorded at each VE: Clear: C, blood stained: B, or meconium stained: M. If membranes r NOT ruptured, record I for intact >> C, B, M, I Moulding: -bones r separated and sutures can be felt easily: o - bones r just touching eachother: + -bones r overlapping ++ -bones r overlapping severely +++ Cervical dilation: at every VE and marked w/ a cross (X) -plotting begins at 4cm: begining of active stage 1. *primips: shoul dilate 1cm/ hour Multips at 1.5 cm/ hour -failure to progress is when this does not OCCUR Descent of head : assessed on abdo palpation > divided into fifths palpable above the pubic bone. Descent is recorded as a circle O at every vaginal examination. Contractions: -Recorded every 30 minutes -normal: conract 3-5 times in 10 minnutes. Avoid contracting too soon to prevental fetal hypoxia. -oxytocin drugs can be recorded as well Vitals: and urinalysis is recorded: -encouraged to urinate every 2 hours: test for protein > sign of pre-eclampsia and acetone > monitor for ketoacidosis from the strains of labour. Medications or fluids given: -particularly in an oxytocin IOL -IV Benzylpenicillin if women is GBS positive > 2 doses 4 hrs apart

Antenatal Care counselling OSCE

Preconception: 1. Pre-pregnancy counselling 2. CST 3. Commence folate 3 m before and 3 m after conception 4. Vacinations should be up to date. -Make sure to get Rubella vaccine > MMR as well as Varicella vaccine: wait 1 month after recieving vaccine before getting preg First Trimester screening: 10w-14w -Dating scan (10w): due date of baby -Non-invasive prenatal test: 10w: blood test > screen for chrom abnor: Trisomy 13,18,21 but not covered by medicare/private: $400 -Nuchal translucency scan 11w: chrom ab > Trisomy 13,18,21. If rx >1 in 50 > genetic counselling -Bloods: Pregnancy Associated Plasma Protein produced 1st by placenta then HCG: Thus check PAPP A and HCG levels -previous Dx of Gestational Dx > do OGTT: thus women at risk get 2 OGTT: 1 now, another one at 24-28 weeeks. -Genetic counselling: discuss invasive diagnostic tests: -Chorionic Villus Sampling: ~12 weeks : confirms Dx of T 13,18,21 -OR -Amniocentesis: 15-20 weeks -20 week Morphology scan: checks baby's position and placenta -24-28w: FBE+ blood group and antibodies + all women get OGTT: Diagnosis of Gestational diabetes if: 1. Fasting >/= to 5.1 2. 1 hr >/= to 10 mmol/l 3. 2 hr >/= to 8.5 -28 and 34w: Anti D injection in RH - mom -36w: FBE, GBS anovaginal swab + whooping cough vaccine *pregnant women during: needs flu shot and whooping cough *before preganncy: get rubella/MMR and varicella vaccine

Unplanned pregnanacy and consultation for termination

Present: 1. Where and why? Can u tell me about how preganncy came about? (Party)Were u trying to have kids? Was it consenual? 2. Who: partner, friend, stranger? Will they be involved? 3. What is ur current attitude between 0 where u want to continue pregnancy and 10 being u are 100% sure u want an abortion? 4. When was first day of ur last mensturation period? LMP? And when was pregnancy confirmed and by what? GO PPDAFS: Past gyne, obstetrics, Personal, PDAFS Past Gynaecological Hx: 1. Sxms: bleeding between periods, ^ed urination, discharge, odor? 2. Dx's 3. Surgery 4. CST: date and result 5. Contraception PObHx: 1. GPA: How many pregnancies, how many births, how many adotpions/miscarriages/ectopics 2. Date of delivery, length of preg 3. Spontaenous/induced/intrumental 4. Vaginal/cesarean 5. Cx's before, during, after PMHX: 1. Medical illness/hospitalizations/surgeries 2. Personal Hx: SADAM W Sleep, appetite, defecation, addiction, micturition, weight changes 3. Drugs Hx: 1. Meds, herbs, recreational, smoke, oh, allergies 4. FHx: medical/gyne conditions, malignancies, cousins 5. Social Hx: -occupation, support network, marital status Management: explain all 3: 1. Keep the pregnancy 2. Adoption 3. Abortion Future: Prevention in the future: discuss contraception: both ongoing contraceptivese, barrier methods, and emeregncy contraceptives.

Rh incompatibility continued

Prevention of red cell isoimmunization > passive immuization > administration of Anti-D -takes 72 hrs for maternal system to begin productio nof its own anti D > so this window defines period for anti-D administration -Need to know how much feto-maternal hemorrhage has occured thus Kleihauer or KB test is important to know how much anti-D to give -AntiD covers any fetal RBC in the maternal circulation > preventing mom from making antibodies. When do we give anti-D? -Routine: 1. 3rd trimester: all RH neg women receive anti D at 28 and 34 weeks 2. Plus after birth: given only if baby is RH positive -Sensitizing event: 1. Bleeding in pregnancy: -termination of pregnancy, miscarriage, ectopic, GTD, APH 2. Traumatic stuff: -maternal trauma: fall, accidents, amniocentesis/CVS Dosing and Kleihauer (KB test) during a sensitizing event: -anything <12 weeks: 250 IU -anything >12 weeks: 625 IU Kleihauer test: assess amount of fetomaternal hemorrhage > tells us how much anti-D to give. -use it in APH. Screening moms: -Rh negative women get 625IU at 28 week and another follow up for c,E and kell antibodies. -Partners karyotype Detection of fetal anemia: -MCA Doppler: fetus w/ anemia have high cardiac output and decreased blood viscosity resulting in taller peaks seen on US >>preducts anemia -Best is fetal cord blood test or amniocentesis: assess degree of fetal anemia and thus the need for antigen neg blood transufion via the cord. -To evaluate the need for fetal transfusion > serial amniocentesis for determination of bilirubin levels in amniotic fluid is needed. Fetal anemia on CTG is >>>>SINUSOIDAL TRACE!!!!!!!!!!! Mx of anemia: -serial US: ongoing US monitoring fetal well being -umbilical cord blood transfusion in severe anemia confirmed w/ MCA Doppler. Invasive and carry rx of miscarriage -consider early delivery.

MirenA IUD (levonorgesterel low dose progesterone): 5 years: Actinomyosis infection risk

Prog > thin endometrial membrane and thick mucus Administered in clinic or surgical intervention in nulliparous women Very effective Benefit: 1. ligher less painful periods 2. Headache, N, mood, bloating 3. Easily return to fertility 4. Best control of heavy periods Cons: 1. Risk of infection or perforation on insertion (actinomyosis infection BUZZ) 2. Spotting first 3-6 months is normal 3. Increase risk of ectopic and miscarriage bc the obstruction in the uterus NEED to wait until 6 weeks post partum to put them in.

Progesterone only: 3 hour window, Missed dose > use barrier for 72 hours.

Progesterone only pill: mini pill -progesterone > supress LH thus No ovulation -Doses have to be a bit higher than IUD or patch bc must pass through GIT. -Thickens mucus and thins endometrium. **Administration for 21 days but this must be exactly at the SAME TIME each day. WITHIN 3 hours. Can be taken anytime, will be protected from preg after 3 days. Use a condom until then. *Must take it at the same time each day. If missed it, then use barriers for3 days until ur back on track. Failure rate: 1.1% if perfectly taken to 13% bc of narrow window Benefit: 1. Used during lactation bc no estrogen that affects milk supply 2. Fertility returns quickly CI's: 1. Pregnancy 2. Liver cancers SEs: 1. Headache 2. Breast tenderness 3. Acne/ hirsutism 4. N/ depression/anxiety/ bloating 4. Spotting

HIV

RNA Retrovirus > infection of CD4 T-cells > inject HIV RNA > reverse transcriptase > HIV DNA > nucleus > forms proteins > HIV buds out -optimal mx can minimise rx of transmission to partner and fetus -If new confirm w/ the ELISA follow up w/ diagnostic western blot. factors that reduce vertical transmission from 30% to 2%: -Maternal anti-retroviral therapy straight away -cesarean section -neonatal antiretroviral therapy - zidovudine for 6 weeks -infant feeding (bottle feeding): only CI to breast feeding that we know. DO NOT BREAST FEED -Antiviral therapy: commence btween before 28 weeks of gestation and continued intrapartum. Delivery: -vaginal recomended if viral load is <50 copies/ml at 36 weeks or else > cesarean section -zidovudine infusion >start 4 hours before begining cesarean. Neonatal antiretroviral therapy ART: -zidovudine > oral > if maternal ivral load is <50 otherwise triple ART should be use. -continued for 4-6 weeks. Fetal cxs: -bc fetus is recieving maternal ABs through placenta > it will be HIV antibody positive for the first 6 months of life making Dx difficult > thus Nucleic acid PCR is used to detec presence of virus and multple negative results confirm absence. -routine antibody serology at 18 m should show no HIV Screen: Antenatal screening with pretest counselling (HIV test): -HIV antibody > screen w/ ELISA and confirm w/ western blot. Ix: -HIV RNA viral load -HIV resistance testing -CD4 + lymphocyte -FBE, LFT, UEC -Other STDs: syphillis, Hep B/C, CT, Low vaginal swab for GBS at 35-37 weeks Mx: NIRS: notify and follow up as high rx, ID referal, reduce transission (ART at before 28 weeks) and screen household contacts

Hepatitis C

RNA virus transmitted predom via blood via unsterile transfusions and shared needles -risk of vertical transmission is 5% unless the mother has HIV > then rx is much higher -similar to hep B > may have chronic infec of hepatocytes > actively infected women > ^er rx of transmission to baby -*In both chronic Hep B and C > may have post partum flares (typical viral prodromal illness) Mx: NIRS: -Notify and follow up as high risk -ID referal -Reduce vertical transmission Delivery: no fetal scalp electrode and avoid instrumental Baby: breast feed is fine in everything other than HIV unless crackled nipples Maternal: new therapy used in 3rd trimester to reduce transmission. 80% r able to clear the virus Screen household contacts. *OSCE: female infected w/ hepatitis presenting in early pregnancy > get hepatic cxs of pregnancy until after 20 weeks and is more likely to be a normal jaundice picture Jaudnice in pregnancy: <20 weeks (early pregancy) > normal DDX for adult jaundice >> Most common: hemolysis, hepatittis A/B/C, cirrhosis, gall stone >20 weeks (later preg): hemolysis, hep A,B,C, cirrhosos, gall stone PLUSSSSSS 1. Cholestasis of pregnancy 2. Acute fatty liver of pregnancy 3. HELLP syndrome

Vaginal Birth After Cesarean VBAC: IPBRAAD

Risks: -rupture of uterus: 5 in 1,000 women - ^'ed rx of mortality and morbidity: more risky for the babies health: ^ed rx of perinatal loss before and during labour and hypoxic injury -^'ed risk of emergency CS: 1 in 4 (remember this) Benefits: -good for future pregnancies -avoid major surgery and anesthetic risks and infection -ealier mobilizaitaon and dc > 1-2 days -gratification of achieving a vaginal delivery.

Antenatal exam: SSSM FUN PIP FAT

Size Shape Striae Movements: A. Primi: 18-20 w B. Multi: 16-18 w. Fundal height -fundus becomes palpable above pubic bone at approx 12 weeks. -from xiphisternum down > fundal pole -fundal height is taken from pubic symphasis = gestation when >20 weeks (umbilicus) Uterine shape Number of fetus Presentation and engagement (Fifths) -ask pt it may be uncomfortable: take deep breath in and out > feel lower abdo > if moveable > then head is not engaged. If not moveable then the head is engaged. -A head which is mobile above the brim > accomodate the full width of five finers. -As head descends, portion of head remaining above brim will represent fewer fingers (4/5 or 3/5 etc) *generally accepted that head is ENGAGED when portion above the bri mis 2 fingers or less Lie: longitudinal, transverse, oblique Position: ROT, LOT, ROP, LOP, OA, PA -anterior fontanelle: 4 sutures > diamond shape and is much larger than posterior -posterior fontanell: triangular shape > back of baby -majority of case: u will feel triangular posterior fontanell Station: Fifths (engagement) Auscultation: FHR: 110-160BPM *always take the maternal pulse to ensure that this is not being auscultated DEPS: Diltation: put finer in see how dilated it is Effacement: is the cervix flattened? Position: feel the scalp of baby: OA, OP etc Station: feel babys head and the ischial spine > if it is at +1 below ischial spine >> can induce labour or vaginal delivery

Intra-Uterine Growth Restriction IUGR

Small for gestational age: GROWTH -fetal weight is <10th percentile on ultrasound. -this Dx doesnt imply pathologic growth abnormalities, and may simply describe fetus is at lower end of normal range. -It may be A. Pathologgical > part of IUGR B. Non pathological: small mom, nulliparous, female babies Intrauterine Growth Restriction: IUGR: can be symmetrical or asymetrical (head sparing): risk factor for pre-term delivery -Fetal weight <10th percentile on ultrasound that bc of pathologic process, has not attained its biologically determiend growth potential -symmetrical IUGR: a/w chromosomal anomalies (trisomy 13,18,21) and w/ fetal alcohol and intrauterine infections (CMV or others) -Asymmetrical IUGR occurs in the 3rd trimester: head is spared >a/w maternal HTN, malnutrition or other maternal conditions Aetiology of IUGR varies w/ time of onset: -1st and 2nd trimester > Symmetrical IUGR > chromosomal anomalies (trisomy 13,18 21), fetal alcohol syndrome and congenital infections (CMV). -3rd trimester > Asymmetrical IUGR (head spared): placental insufficiency (maternal HTN, malnutrition) and other conditions other causes: maternal: -GDM, Thyroid, Lupus, autoimmune disease, cardiovascular disease, COPD -smoking, Oh, drugs (cocaine) -nutrition: under nutrition, or obese mom -nulliparity: first term preg r a/w ^ed IUGR -hypoxia: due to anemia, altitude, chronic resp distress. Fetal: -multiple gestation -chromosomal anomalies: trisomy 13,18,21 -TORCH infections: Toxoplasmosis, Other (syphillis), rubella, CMV, herpes/HIV r a/w low fetal weight -transverse fetal lie is a/w IUGR Placenta: -Pre-Eclampsia: leads to placental insufficiency > IUGR baby -Abnormal placental anatomy: A. Idiopathic B. single umbilical artery C. Placenta Previa: low lying 7 o clock D. Placenta Accreta: embeded into myometrium -Cxs: growth restricted babies r likely to suffer: A. Antenatal and intrapartum still birth B. Neurocognitive deficits C. Long term health problems in childhood and adult life. **** as birth weight centile decreases, perinatal mortality increases. -<3 centile birth weight > more than 50% perinatal mortality and mobidity Low birth weight: -Low <2.5 kg -Very low <1.5 kg

Stage 1 of labour: NP: <8 hours MP: <4 hours

Stage 1: -latent stage: 0-4 cm: dilation of cervix reduces support for fetal amniotic membranes > bulges through cervix > often rupture of these membranes > initiate active labour Mx: consider antibiotics in GBS positive owmen > 2 doses of IV Benpen 4 hours apart. Active phase: 4-10 cm -this is when we start monitoring labour on partogram -nulparrous: 1cm per hour -multigravid: 1.5 cm per hour Mx: -regular monitoring of progress -fetal HR every 30 min > either auscultate or CTG when high rx -maternal obs and VE every 4 hours > speed of dilation is important to monitor but weigh it up against rx of infection. Transition: -set of behaviors which represetns transition from first to second stage of labour -feelings of loss of control, irrational, request more pain relief *Active stage -Nullparious:: <8 hours -Multiparous: <4 hours

Partogram

Stage 1: Latent phase -primip >8 hours -multi >4 hours Means prolonged labour. Stage 1: Active phase: When cervix reaches 4cm > active phase of stage 1 begins: document on partogram + 4 hrly VE -Cervix should dilate at: Nuliparous: 1cm/hr Multigravid: 1.5cm/hr Prolonged first stage >>Induction of labour: Bishop score also known as cervix score is a pre-labor scoring system to assist in predicting whether induction of labor will be required. It has also been used to assess the likelihood of spontaneous preterm delivery. -contains DEPS C: dilation, effacement (how thin cervix is) , position (posterior, middle, anterior), station (-3,-2,-1/0, +1/+2), consistency (firm, medium, soft) -highest score is 13, lowest score is 0. ->8 can induce labour w/ amniotomy or oxytocin infusion - < 8 need to prime the cervix: can be done w/ prostaglandins or w/ foley catheter. -can either use prostin gel, cervadil pessary or oral misoprostol > then see if this chagnes cervix (this often induces labor itself) and then proceed to amniotomy or oxytocin induction. Proloned second stage >> Instrumental delivery -indications: delayed 2nd stage of labour. Requirements: FORCEP: -favorable presentation: head must be engaged >0 station -O: Os fully dilated -Ruptured membranes -contractions present: delivery is assisted by contractions and ^ rx PPH -Episiotomy if req -pain control Procedure: -Ventous: cup is placed on the vertex (over the posterior fontanel) > and when inflated > can allow traction A/w slightly higher fetal cxs. Suction causes > swelling in the scalp -Forceps: 2 piece clamp that is inserted into the vagina and allows grasping of the fetal head> Head must be in OP or O position -a/w ^ maternal cxs.

Recording of contractions

Stage 1: contractions last btwn 30-60 seconds -Latent stage: 2-3 contractions/10 minutes -Active and transition stage: 4-5 contractions in 10 minutes Stage 2: last approx 90 seconds -4-5 contractiosn/10 minutes. Exchange of gases btwn fetus and mom is stopped during each contraction when intrauterine pressure exceeds >30mmHg > causes block in placental blood flow. *uterine hyperstimulation: tachysystole: >5 contractions in 10 minutes may limit refilling of placental and fetal circulation >> fetal hypoxia *hypertonus: each contraction lasting >2 minutes.

Stage 2 of labour: NP: <2 hours MP <1 hour: +1 hour if if epidural

Stage 2: -10 cm dilation to delivery of baby Passive Descent: passive > baby moves down pelvis w/o conscious control from mother. Takes approx 1 hour. Active pushing: -overwhelming urge to push > "Ferguson Reflex" > a positive feedback loop promoting delivery of fetus. -sensory afferent neurons on cervical smooth muscle and on the smooth muscle of rectum r stimulated by distentttion of fetal head > brainstem > supra optic and PVN of hypothalamus > release oxytoci ninto posterior pituitary > into circulation -Oxytocin directly and indirectly (via prostaglandins) increase contractility of myometrium. *Strong bearing down reflex (valsalva to push baby out): during second stage of labour > compression of bladder and rectum generates a reflex that causes bearing down or urge to push. -bearing down (urge to push) can occur prior to full cervical dilation > can risk a cervical tear and lengthen ligaments supporting the cervix. *Thus encouraged not to bear down until cervix is fully dilated (10cm) Mx: -close monitoring of progress due to ^ likelihood of cxsm. 1. Estradiol from placenta redies uterus for response to oxytocin (^s oxytocin receptors on myometrium) 2. Head pushes agianst cervix > activates stretch sensitive sensory neurons > hypothalamus > oxytocin from post pituitiary > stimulates stronger uterine contractions 3. Prostaglandins secreted by uterus also enhance contractions. -Dont Flex In ER: Descent, flexsion, internal rotation, extention, restitution. Suboccipital bregmatic SOB (OA) is the best way and smallest. -Administer oxytocin the moment babys anterior shoulder is out > prevent PPH -Occipitomental is the largest diameter. Management of second stage: -regular monitoring -similar to first stage in that fetal HR should be recorded after every contraction or atleast every 15 minutes > map on partogram ******Duration: Nulparrous <2 hours Multiparous <1 hour *+1 hour w/ epidural

Pharmacological analgesia

Step 1: Inhaled nitrous oxide mixed w/ O2 > moderate analgesia in 50% of women. -rapid onset and offset thus used during contractions A/E: headache, sedation, dizziness, N/V Step 2: IM pethadine: opioid -100mg Pethadine (short acting opioid) commonly used as step up therapy after gas -cause fetal adverse effects > respiratory suppression thus we only give pethadine at a dose we are not guaranteed to get results at bc we need to avoid harmful levels for baby -provides adequate relief in upto 25% of women AE: maternal: N/V/sedation, neonate: respiratory suppression, restless, impaired initial breast feeding, hand and mouth movements Step 3: Epiduural anesthetic: -implanted sacral catheter > allows ropivicaine/bupivacaine PLUS fentanyl into epidural space at level of S2-S4 -touching above pelvic pain line (uterus> visceral pain) > follow Sympathetics: pain and sensation of contractions are above PPL thus follow sympathetics >> missed by epidural and these sensations are maintained. -Below pelvic pain line (cervix and vagina) > cause shallow visceral pain> follow the PSNS: thus pain in cervix, vagina, perineum is reduced while ability to feel contractions. Thus remain actively involved in delivery and lower rx of atonic PPH *works within 10 minutes to take full effect 4. Others: A. Sterile water injections: 4 water injections r given SC over the llumbar spine -very painful > provides good short term relief 60-90 mins B. Perirectal Diclofenac: -PR voltaren is commonly used in pts w/ vaginal lacerations that need to be sutured -PR or PV delivers the meds directly to site of inflammation > good analgesia i npost partum period.

Urinary Sxms: Irritative FUND VS obstructive SHED (BPH)

Storage FUND (bladder): 1. Freq 2. Urgency 3. Nocturia 4. Dysuria: pain or burning while urinating Voiding SHED > Obstructive (BPH or prolapse) 1. Stream: low 2. Hesitancy 3. Emptying incomplete 4. Dribbling

Moulding VS Caput succedaneum VS Chignon

The bones of the fetal head can move closer together or overlap to help the head fit through the pelvis. Parietal bones overlap occipital and frontal bones. Moulding can decrease the biparietal diameter by ~1 cm. Significant moulding (with caput) can be a sign of cephalo-pelvic disproportion and this should be ruled out before attempting an instrumental delivery. What is normal? Up to 2+ occipito-parietal moulding may be normal in the later stages of labour. No moulding: parietal bones r not overlapped +1: parietal bones r touching but not overlapped +2: parietal bones r overlapped but can be reduced: forcep may be better than vaccum esp if there is signif caput +3: pareital bones r overlapped and cant be reduced. Severe parieto-parieto moulding is never normal >>cephalopelvic disproportion -need CS *Caput succedaneum: swelling, or edema, of an infant's scalp that appears as a lump or bump on their head shortly after delivery. This condition is harmless and is due to pressure put on the infant's head during delivery. It doesn't indicate damage to the brain or the bones of the cranium Chignon: swelling on babys head after ventouse

What causes preterm labour?

There is a balance btwn prodelivery (estrogen) and progestation (progesterone) -when Estrogen ^'s: get 1. ^'ed oxytocin receptors on myometrium 2. ^'ed gap jxns on myometrum 3. Cervical ripening >> softening of cervix > begins prior to onset of labour contractions and is needed for cervical dilation and passage of fetus. Cervical ripening results from changes in collagen. Cervix thins, softens, relaxes and dilates in response to contractions * with uterine contractions > ripened cervix (soft cervix) dilates as fetus descends *In the case of rupture of membranes > releases prostaglandins over the cervix > stiumulates dilation and effacement. Normally: contractions causes cervical dilation and effacement For preterm delivery to occur > cervix underoes collagen breakdown and altered proteoglycan and water content >>effacement and dilation 1. When the lower segment stretches, there is cervical change > mediated by influx of inflammatory cells releasing metalloproteinases 2. Increased contractility of the upper segment is a/w expression of prostaglandin, oxytocin receptors, and gap jxns. *Progesterone may be anti-inflammatory thus used as a prophylactic tx *Infection also causes inflammation which can lead to dilation and effacement >>preterm labour.

Baseline Complications of the Puerperium:

Thromboembolism: -largest cause of maternal mortality in post partum period just w/ PPH -very high rx from low mobility > engorement and stasis of pelvic veins, -Women should discontinue anticoagulation therapy before spontaneous labour occurs and not take LMWH 24 hours before getting epidural. DVT: -Painful, red, swelling in thigh/calf -may become pale or purple as welling progresses PE: -pleuritic chest pain -acute onset SOB -cough +/- PINK FROTHY SPUTUM -collapse - High HR and Low BP Ix: -ECG: S1Q3T3 trace. -SO2 +/- immediate O2 -FBE, ABG, Coags -Doppler of leg veins, CTPA (gold standard), V/Q scan. Mx: Prevention: -compression stockings -early mobility -clexane: post cesearean, or ^ BMI Mx: 1. Supplement O2 2. Anticoagulation: LMWH (Clexane) +/- long term anticoagulation on warfarin (breast feeding fine) 3. Thrombolysis: not recommended w/ 10 dayys of delivery.

Syphillis

Treponema pallidum: spirochete bacterium -more common in rural, indigenous ppl -Maternal infection: Primary infection: -active infections presents as raw painless ulcers on genitals Secondary infection: dissemination of bacterium can result in development of macular rash over the palms and soles + muscle aches and pains + fever. Sub clinical infection: following this period > infec can be asymptomatic and only identified by serology Tertriary infection: expansion of bacterium from sub clinical state is rare > but involve nervous tissue, heart, and major vessels + mucosal surfaces. Fetal cx: -super rare -congenital disease > development abnormalities: A. Snuffles: nasal d/c B. Saddle nose: nose is pushed back w/ saddle apperaance above C. Saber shins: tibia and fibula arched in AP plane D. Skin lesions: blisters and ulcers on baby Hutchinsons teeth: notched incisor teeth, keratitis, 8th nerve deafness. NIRS Mx: -notify and f/o as high rx -ID -reduce vertical transmisison: ABx: benzathine Penicillin IM 3 doses weekly. In penicillin allergeric > do desensitization then give IM Ben pen.

Multiple Pregnancy

Twins r most common form of multip pregnancy 97% types of twins: Identical: monozygotic twins: sperm > egg >> the ovum splits and forms 2 identical fetus with same placenta. Rx of TTTS Fraternal twins: Dizygotic twins: 2 eggs released > sperm penetrates it > 2 different placenta: occurs from IVF/fertility drugs/hereditary Epi: 1% of all pregnancies in Aus -97% twins, rest r triplets RFs: 1. Poly ovulation: likely to occur w/: ^ maternal age, maternal FHx, ^ed parity (births) > ^ rx of dizygotic twins 2. ART (assisted reproductive technology) IVF: multiple embryos r inserted into uterus: ^ rx of both attaching >dizygotic twins -ART is the only rf that ^'s rx of monozygotic twins > can split during early development. 3. Clomiphene citrate: used in anovulatory infertility (PCO) ^ rx of dizygotic twins bc it too will ^ rx of polyovulation *Polyovulation > dizygotic twins *ART ^'s rx of Monozygotic twins (higher rx of feta cxs) and dizygotic twins Amnion: inner membrane: which holds amniotic fluid around the babay: easy to remember which is on the inside) > formed by formation of a cavity w/in the inner cell mass -amniotic cavity contains amniotic fluid > surrounds and cushions developing fetus Chorion: combination of mesoderm and trophoblast. -chorion is formed by trophoblast and then mesoderm. Importantly > chorion continues INTO the placenta thus twins that r monochorionic r going to share the same placenta bc they share the same chorion. umbilical cord: contains portion of allantois (outpocketing of endoderm near base of yolk sac), BVs and remnants of yolk stalk. *fetal part of placenta is chorion, maternal component of placenta is decidua basalis. Dizygotic twins: pregnancy is: -dichorionic: 2 separate chorion and placentas -diamniotic: 2 separate amnion Monozygotic twins: depends on time of splittin of embryo: -Day 0-3 > dichorionic diamniotic pregnancy -Day 3-7 > monochorionic diamniotic pregnancy -Day 7-14 > monochorionic monoamniotic pregnancy - >14 days > monochorionic and monoamniotic PLUS conjoined Hx: -large fundal height -hyperemesis gravidarum bc of higher level of BHC: Severe early onset hyperemesis may be a/w multiple preg -accerelated weight gain -abnormally high BHCG: VERY high BHCG is a/w GTD or Twin pregnancy. -2 fetal Heart sounds To confirm the diagnosis of twins > first trimester ultrasound >> -Lamda sign (Triangle) > on US suggests Dichorionic twins: best seen btwn 10-14w. -T signs > monochorionic diamniotic -No sign > absence of amniotic division btwn the twins suggest monochorionic monoamniotic

Structural

Uterus: 1. Have you ever had an ultrasound of the pelvisor hysteroscopy? A. Submucosal fibroid: benign tumor of myometrium (leiomyoma). Physical obstruction of uterine cavity or ovarian tuube may prevent fertilization B. Endometrial polyp: dysplastic cells arise from glandular endometrium. 2. Previous curettes? > Synaechiae: AKA Asherman's Syndrome: where fibrous adhesions form wi/in uterus and prevent fertility. Tubes: -Silent PID: when infections ascend into uterus and ovarian tubes > they disrupt epithelial layers and promote adhesions. Q's: previous Hx of STI/recent cehck? Stinging, burning with urination? D/c or abnormal smell? -Perforated appendix: mediate ovarian/tubeal damage/adhesions Q's: PmHx: of appendicitis? -Endometriosis: production of abnormal endometrial tissue on outside of uterus. Worry about phyiscal obstruction of the ovarian tubes or ovary preventing fertilization/implantation Q's: : Cyclic pelvic pain? Dysmenorrhea? (Menstrual cramps) Dyspareunia? (Painful sex) Others: Thyroid: -both hyper/hypothyroidism can be a/w anovulation and decrease in chances of preg. Both will cause secondary amenorrhea. MONASH: only get amenorrhea in hyperthyroidism. Q's: weightloss, heat intolerance, tremor. Or weight gain, cold intol or tired/weak

Instrumental delivery

^ prevalence w/ ^ epidural analgesia: "lift out deliveries" > caused by effects of analgesia preventing ability to push. indications: all arise in second stage of labour bc the fetal head needs to be below 0 station 1. Prolonged second stage of labour: -primip: 2 hours -multi: 1 hour *+ 1 for epidural. -prolonged second stage ^s rx of cxs for both mom (compression of perineal structures) and baby -2nd stage ^'s rx of fetal hypoxia when: A. Theres ^ contraction of uterus > thus blood flowing through spiral arteries to placenta and baby is reduced for longer time B. When theres cord compression > as baby descends further into pelvis. The longer we leave baby exposed to this > greater the rx of cxs. 2. Fetal compromise: determined by CTG -when fetal head has descended to 0 station (engaged) the pt is taken to theater for trial of forceps w/ the option of CS if unsuccessful. 3. Mom not able to push: -need uterine contraction and ability to push. -might not want her to push in: severe HTN/PET, known cerebrovascular malformations, marfans syndrome (rx of aortic dissection) -she may not be able to : uterine exhaustion after prolonged labour, extension of epidural anesthetic 4. Vaginal breech delivery:

Normal labour

attitude: refers to posturing of joints and relation of fetal parts to one another. Normal fetal attitude when labor begins is w/ all joints in flexion Presenation: cephalic or breech Lie: longitudinal, transverse, oblique Position: point of reference of occiput in relation to eight octanes of pelvic inlet > ROT, LOT, OA etc Station: how far down is babys head descended down the pelvis. Zero point is the ischial spines. Above that it is negative 5. Below that is positive 1, 2, 3, 4, 5. -Negative 5 station > pelvic inlet > floating -neg 4 -neg 3 -neg 2 -neg 1 -0: ischial spine > this is when the baby is engaged (labour begins) +1 +2 +3 +4 +5 : pelvic outlet > crowning -Engagement: put hand on lower abdomen and grab the head of the baby, if it is mobile > it is not engaged (0/5ths). If engaged > check for how many fifths Progesterone: Pro Gestation: -dilates spiral arteries > maintains endometrium. -relaxes smooth muscle contractility of A. Myometrium: preventing fetal disruption B. Vascular: controlling BP under high circulatory volume C. Gastrointestinal: decreases contractility > can cause constipation Estrogen: Promotes delivery -maintains cells of endometrium > support fetal growth -Promotes contractility o futerus by ^ing number of oxytocin receptors in myometrium > thus EST rises above PROG in later final stages Cortisol: -before giving birth. > Neg feedback for ACTH/Cortisol in hypothalamus is ignored allowing high cortisol levels to help final maturation of fetus (lung, gut, kidney, HgB) Elastin: released > increases stretch of connective tissues and ligaments of pelvis By 26-28 w get stretching of lower uterine segment -Pre term > cervix remains firm, long and non compliant, its outlet is sealed by mucus plug to prevent ascending infection -cervical ripening >> preparing for delivery allows: A. Effacement: shortening of cervical length B. Dilation: dilation of cervical opening Factors that promote dilation and effacement: -prostaglandins: PGE2 and PG promotes cervical ripening and dilation