Obstetrics — USMLE Step 2 CK Notes

Endometriosis: Uterus not enlarged

Bleeds into peritoneal cavity

DYSMENORRHEA and dyspareunia -> Only painful sex during menstruation

Can displace cervix

Cervical motion tenderness

RF: Nulliparity and low BMI

NB not abnorm proliferation but abnormal place! Can cause INFERTILITY —-> disrupts pelvic anatomy/oocyte release/sperm entry

Tx: NSAIDs +/- oral contraceptives, mirena ; GnRH

Cauterisation (adhesions) or removal of ovaries (takes hormones away)

Uterine Polyps: Light AUB: Norm sized uterus Pedunculated fleshy growth

Calcified (can resemble fibroid)

Hyperechoic

AUB: Doesn’t affect ovulation

—->> Regular menses with light Intermenstrual bleeding: d/t friability and vascularity

Fibroids: Irregular sized, bulky Enlarged Uterus Proliferation of SM within myometrium

Typically cause regular (ovulatory) but heavy, prolonged menses: Menorrhagia Can cause AUB

Growth increased by oestrogen, pregnancy, OCP

Globular masses

Can cause breech -> submucosal

Adenomyosis: Symmetrically (diffusely) Enlarged, boggy (soft) uterus Endometrial glands within myometrium

Menorrhagia and dysmenorrhea -> No intermenstrual bleeding

Tx for AUB:

IV estrogen or high dose OCPs to stabilise endometrium; High dose progestin if estrogen CI

Third Trimester Bleeding

Placenta Previa

Abnormal implantation (Hx)

Placenta grown across the os -> When cervix dilates placenta attached so tears

Reassuring fetal monitoring initially

Dx: Transabdominal followed by TVUS

Management: No sex; No. digital cervical exam; Inpatient admission for bleeding episodes

RFs: Previous Placenta Previa; Prior caesarean

Multiple gestation (increased placental surface area); Adv maternal age

Most cases resolve spontaneously by trimester 3

If persistent pts undergo caesarean delivery at 36-37wks

Vasa Previa

Blood vessels connect uterus to accessory lobe

—->> bvs lie across Os——>> tear when cervix dilates —->>>>> fetal exsanguination

Dx: NTS ——->> Fetal Distress: bradycardia and sinusoid all pattern

Tx: Urgent C Section

Uterine Rupture

RF: Previously scarred uterus (C Section); Oxytocin—->> forceful contractions

Loss of fetal station: 0-> -3

Fetal HR: Uterine rupture if 80bpm at nadir (bradycardia): Peak to Nadir >30sec —>>> Sudden decrease in HR W prolonged fetal HR deceleration: Mother will have increasing lower abdo pain, vaginal bleeding not necessary

Can cause fetal parts to partially expulse into maternal abdomen

——>> palpable irregular abdominal protuberance ===> No vaginal mass (cf inversion) ## Tx: Crash C Section

Vaginal hematoma

RF: Operative vaginal delivery; Infant > 8.8lb; Nulliparity; Prolonged 2nd stage of labour

Vaginal purplish mass +/- hypovolemic shock

==> blood collects in paravaginal potential space so minimal external bleeding but huge blood loss

Tx: Nonexpanding -> observation

Expanding -> embolisation, surgery

Uterine Inversion

RF: Nulliparity; macrosomnia; Placental accreta; rapid labour and delivery D/t excessive fundal pressure and traction on umbilical cord b4 placental separation

Smooth round mass protruding through vagina/cervix; massive postpartum hemorrhage and

hypovolemic shock w lower abdo pain

Uterine Fundus no longer palpable transabdominally (cf rupture)

Management: Aggressive fluid replacement; manual replacement of uterus

Placental removal and uretotonic drugs after replacement

Placental Abruptio (think of this as fetal and maternal). PAIN WORSE

Placenta tears off endometrium but placenta stays in

Pain can be in the back or abdo

Blood uterotonic —> firm uterus w unusually low amplitude high frequency contractions

Sometimes placenta can remain attached so as to conceal the bleeding

—> causes uterine distension (fundal height larger cf expected)

Large force needed to rip placenta off: HTN/COCAINE; MVA

Hx of smoking

Tender, hypertonic uterus

Dx: US/NTS

Kleihauer-Betke test for fetomaternal hemorrhage in setting of placental abruption

—->> determines necessary dose of anti-D Ig after delivery of Rh+ foetus to Rh - mum

Decelerations (of fetal HR) during labour: VEAL CHOP

Early decelerations: head compression

Late decelerations: fetal hypoxaemia and forceful contractions (stop oxytocin)

Give mother O2 and change position —>>> left lateral with legs raised

IV fluids to counteract dehydration

Variable decelerations: Common when foetus descends into birth Canal

Abrupt in decline and return to baseline (<30s cf uterine rupture)

Cord compression/abnorm position (can cause reduced fetal blood flow) Cord compression w <50% contractions well tolerated: no hypoxia

Recurrent variable decelerations in w > 50% contractions

—-> maternal repositioning to reduce cord compression

—-> amnioinfusion if no improvement —> reduces compression

Most ominous when repetitive and severe (below 60bpm): if recurrent then Caesarian!!!!

Prolonged deceleration if decrease of 15 bpm below baseline for 2-10 minutes

Sinusoidal tracing : severe hypoxia eg in Vasa Previa and Rh disease

Umbilical cord prolapse: Abrupt, prolonged deceleration or bradycardia

Contraception

Long Acting Reversible Contraception: most effective even cf tubal ligation/vasectomy

Non IUD: Subcutaneous —-> lasts 3 years

Etonogestel (progesterone) arm implant more effective than even IUD

—> irregular bleeding/spotting for initial 6 months or more

IUD: CI to IUD: Acute pelvic infection; Severe uterine cavity distortion; AUB; Wilson disease

Hormonal —-> last 5 years; CI Current breast cancer; can cause irregularity

Copper —->> longest acting (10 yrs)

Moderate efficacy: Descending order of efficacy and duration

Injections: 3 months

Patches: E+P—> Highest risk of DVT/PE

Rings: E+P —> min breakthrough

OCPs: Inhibits LH surge -> no ovulation; metabolised via P450

Used in pathologic states: AUB/Choriogestational trophoblastic disease/Molar prev

Mini Pill (Progesterone only): Daily compliance down to the hour needed

Low efficacy: Condoms and diaphragms: Diaphragm > Cup

Hysteroscopic Sterilisation

Insertion of nickel into FTs ——>> gradually cause scarring but can take 3 months

—->> must use back up birth control until then

Contrast media used in hysterosalpingogram to confirm occlusion

CI: Previous tubal ligation; allergy to contrast media/nickel; uterine/FT pathologies;

recent/active pelvic infection

OCP combo pills

Inhibits LH Surge

CI: >35 if smoking >15 cigarettes per day; SLE; Migraine w Aura; breast cancer; cirrhosis;

RF for CV Disease inc DM and HTN; thromboembolism; Hx of stroke, Hepatocellular adenoma

Oestrogen containing contraceptives CI <1 month postpartum -> increased risk of thromboembolism

Medroxyprogesterone acetate Injection

Thickens cervical mucus; decidualises endometrium -> atrophy; impairs Tubal peristalsis

Osteoporosis risk in over 35s

Progestin only IUD does not affect thrombotic state -> systemic forms still not used in high risk pt Protective against endometrial cancer

Oestrogen only contraception is CI in breastfeeding as can decrease milk production

Emergency Contraception

Copper IUD. 0-120hr. >99% effective.

Ulipristal (Progestin R blocker). 0-120hr. 98-99% effective —-> delays ovulation

Levonorgestrel. 0-72hr.

High dose OCPs. 0-72hr.

Oestrogen-progestin Contraceptive (inc rings): Pros/cons

Benefits: Endometrial and ovarian cancer risk reduction

Menstrual regulation; Hyperandrogenism tx (acne, hirsutism)

Risks: Thromboembolism; HTN; Stroke; MI

Hepatic adenoma

Cervical cancer; Moderate breast cancer risk

Mood changes due to combined pill mainly Due to progesterone

Primary Amenorrhea: genetic/anatomical Absence of menarche in girls aged 13 or older with no secondary sexual characteristics

Absence of menarche by 15 w secondary sexual characteristics

Pelvic US to check for Uterus:

Absent Uterus: Karyotype: 46 XY AI

46 XX Mullerian Agenesis: has ovaries

Uterus Present: Check FSH:

Low FSH: Cause is Central:

—->>> Hypothyroidism; Prolactinoma; Functional Hypothalamic Amenorrhea (FHA),

Cushings Syndrome (glucocorticoids suppress GnRH)

Norm FSH: Imperforate Hymen

High FSH: Cause is Peripheral: Lack of oestrogen and Inhibin -> Lack of Feedback Inhibition

—->>> Check Karyotype: 46XX Primary Ovarian Insufficiency or 45XO Turners

Mullerian Agenesis (Mayer-Rokitansky-Kuster-Hauser Syndrome): MCC

Abnorm development of uterus, cervix and upper 1/3 vagina

Norm secondary sexual characteristics eg pubic hair and stature

Absent uterus and upper vagina -> 46XX with intact ovaries -> Hormonally normal

Management: Evaluate for renal tract abnormalities (renal US); Vaginal dilation

Androgen Insensitivity Syndrome (defect in androgen receptor: no DHT effect)

Normal appearing female -> Decreased pubic and axillary hair w Increased height

46XY produce MIF (degeneration of internal female sex organs) -> NO OVARIES

Presence of intraabdominal testicles (crytorchid)

Increased testosterone and LH (R) and estrogen (aromatase conversion of testosterone)

5-alpha reductase deficiency: Virilisation at puberty d/t increased testosterone

46XY, phenotypically F at birth

Impaired testosterone to DHT conversion; Norm male testosterone and estrogen levels

Male internal genitalia -> no uterus etc

F ext genitalia: blind ending vagina.

Maternal virilisation: Aromatase deficiency in foetus (inability to convert DHEAS to estrogen)

Mother gets excess androgens: hirsutism

Child has norm internal genitalia w ambiguous ext genitalia at birth

Delayed puberty, osteoporosis and undetectable oestrogen levels

High gonadotropin ====> Polycystic ovaries

Turners Syndrome

Increased risk of aortic dissection d/t bicuspid AV —> risk increases in pregnancy

Short stature; webbed neck; scoliosis; micrognathia; cubitus valgus

Renal and Ovarian disorders common

Abnormal Uterine Bleeding

Immature HPO Axis (after recent menarche)

Not enough FSH and LH produced to induce ovulation: anovulatory

Painless, irregular, heavy bleeding:

Unopposed estrogen as no progesterone (no corpus luteum)

Endometrium keeps on proliferating until it outgrows blood supply

Tx: Progesterone to stabilise endometrium or combined oral pill to help regulate menses

Progesterone Challenge

Withdrawal bleeding suggests amenorrhea due to anovulation (endogenous Estrogen present)

Estrogen challenge if progesterone challenge negative

Withdrawal bleeding signifies lack of Estrogen is the issue

No bleeding signifies obstruction

Adhesions -> lack of endometrial tissue and no bleeding on progestin or estrogen challenge

Maternal Oestrogen Effects in Newborns -> transplacental oestrogen exposure

Breast Hypertrophy (M/F); Swollen Labia; Physiologic Leukorrhea (whitish vaginal discharge)

Uterine withdrawal bleeding

——>> ALL NORMAL and transient (first 2 wks of life)

Testes: Testes should descend by 6 months

Hypospadias (inferior) -> Ventrally displaced urethral opening

D/t incomplete fusion

Dorsal hood appearance

Penile curvature

Karyotype and US analysis if severe:

Urethral opening on perineum/scrotum

Underdeveloped and curved penis (chordee)

Cryptorchidism

Can represent virilisation of XX or undervirilisation off XY

Pelvic US to evaluate internal genitalia

Torsion of appendix testes: Classic ‘blue dot’ pathognomic sign

Pain gradual in onset cf testicular torsion

Tenderness localised to anterosuperior testis

Tx is conservative as resolves in 1-2 wks: Rest, Ice and NSAIDs

Peyronie Disease

D/t repetitive blunt trauma to penis during sex with aberrant wound healing

Fibrous plaques d/t TGF1 upregulation

Penile pain, curvature and dorsal nodules/plaques

Spontaneously resolves in 1-2 yrs in most

Tx: NSAIDs for pain; pentoxifylline to reduce fibrosis and/or intralesional injections of collagen

Surgery

Penile Cancer

Bowen disease: Cutaneous SCC in situ

Penile shaft -> Painless, erythematous plaque

Can progress to cancer: Painless ulcer/nodule with inguinal LAD (>60yrs)

Distant spread rare until late

RF: HPV; phimosis; cigarettes

Varicocele -> Does not transilluminate

Decreased fertility and testicular atrophy

Most common on left

——-> always check for left renal cell cancer as can compress and cause d/t drainage angle

Tx: Gonadal vein ligation (boys and Y men with testicular atrophy)

Scrotal support and NSAIDs

Spermatocele

Cystic epididymis accumulations of sperm that form superiorly to testicle

Usually asymptomatic

Hydrocele: Transilluminate

Collection of serous fluid between layers of tunica vaginalis (surrounding testicle and spermatic cord)

Most asymp and painless

Non communicating in adults: Cancer/infection (mumps/epididymis)/trauma

Communicationing kids: Incomplete closure of processes vaginalis

Hematocele: Testicular trauma

Blood accumulation in tunica vaginalis; Pain

Erectile Dysfunction Causes

Vascular: decreased penile blood flow; endothelial dysfunction and vasoactive medications

Neurological: Comorbidity eg diabetic neuropathy, MS, Spinal injury/surgery

Gradual onset, loss of bulbocavernosus reflex

Psychogenic: Norm non sexual nocturnal/morning erections

Endocrine: TSH/Prolactin; Hypogonadism

Medications: Antihypertensives; SSRIs; Antiandrogenics

Breast

Mastitis: Flu like sx + fever; wedge shaped redness; purulent discharge

Dicloxacillin to cover MRSA and penicillin resistant Staph

Breast Masses: Work up: Palpable breast mass (EVEN FIBROADENOMA)

Age <30 ——>> US (differentiates solid from cystic masses) +/- Mammogram

————->>>> Complex cyst/SOLID mass —->> Biopsy

———->> Simple cyst —-> aspirate (FNA)/nothing

Age >30 ——-> Mammogram +/- US ——-> Suspicious for cancer —->> Biopsy

RF: Modifiable: HRT; Nulliparity; alcohol

Nonmodifiable: White race; early menarche/late menopause

Protective: Exercise and Breastfeeding

Fibrocystic Changes of Breast: Diffuse, bilateral premenstrual tenderness

Tx: OCPs; danazol; NSAIDs

FIBROADENOMA: Cyclic, premenstrual tenderness

Fat necrosis: Firm irreg, nontender mass +/- ecchymosis/nipple retraction

Breast cyst: +/- tenderness

Galatocele: Benign milk retention cyst

Occurs a few wks after cessation of breast feeding when milk stagnates

Can occur during lactation and Tri3

Dried, deposited proteins in lactiferous duct cause blockage

—-> milk backs up ==> soft, mobile nontender mass as large as 5 cm

Phyllodes tumour

Hard to DDX from FIBROADENOMA —> larger and greater metastatic potential

Classic leaf like appearance on histology

Paget’s disease of Breast

Ductal carcinoma (usually adenocarcinoma)

Erythematous, scaly or vesicular rash affecting nipple and areola

Pruritis, burning and nipple retraction

Lesion eventually ulcerates: blood tinged discharge

Can be mistaken for eczema

Intraductal papilloma: No associated mass or LAD

Physiological Galactorrhea

Bilateral and guaiac negative w/o signs of malignancy

Hypothyroidism, chest wall/nipple stimulation (surgery/trauma/shingles)

Dx: TSH and Prolactin levels; Imaging

Inflammatory Breast Carcinoma

Edema, diffusely warm, dimpling, Peua d’orange

Painful; Rare and aggressive

Itching, palpable mass and nipple changes may be present

Axillary LAD if metastases

Tx of Breast cancer: SERMs ## Tamoxifen

Agonist at endometrium and bone

Antagonist at breast

Risk of venous thromboembolism; endometrial cancer

Induces menopause

Raloxifene

Antagonist at breast and endometrium

Agonist at bone (used to tx osteoporosis in menopausal F)

Risk of venous thromboembolism

Induces menopause

Breastfeeding CI

Active untreated TB; HIV infection; Active varicella infection; Herpetic breast lesions

Chemo/radiation therapy

Active breast bleeding if HEP C

Active substance use

Infant has galactosaemia

Exercise CI in pregnancy in conditions: Increased risk antepartum bleeding eg placenta previa

Risk of preterm delivery eg insufficiency

Certain conditions that could be exacerbated by exercise eg preeclampsia; severe anaemia;

Cardioresp Disease

Shoulder Dystocia

Failure of usual obstetric manoeuvres to deliver fetal shoulders

Macrosomnia risk factor

Management: BE CALM

Breathe; don’t push

Elevate legs & flex hips, thighs against abdo (McRoberts)

Call for help

Apply suprapubic pressure

EnLarge vaginal opening with episiotomy

Manoeuvres: Replace fetal head into pelvis for C Section (Zavanelli)

Cephalopelvic disproportion

Failure to progress in labour —> common cause is fetal malposition

Arrested second stage (no fetal descent after 3 hrs or 2 in multiparous)

RF: Macrosomnia (main factor): fetal weight >4.5kg/9.9lbs

Maternal obesity etc

Warning Signs: Protracted labour (pre arrest)

Turtle Sign: retraction of fetal head into perineum after delivery

Tx: C section

Amniotomy only done in Active stage of Labour ????

Hypotonic Contractions

Failure to progress in Labour (>6 hrs post 6cm dilation)

Montevido Unit: Adequate = 200 Units

Fetal malposition: occipital anterior ideal

HTN and short interpregnancy interval risk of growth restriction:

HTN -> underdevelopment of spiral As-> placental insufficiency

SGA, low muscle mass, low sc fat, peeling skin and thin umbilical cord (baby looks ‘wizened’)

Small for Gestational aGE (SGA)

Complications: Hypoxia; meconium aspiration; hypothermia; Polycythemia

LGA: Risk of hip subluxation d/t intrauterine deformation

Neonatal Thyrotoxicosis

Tx: methimazole + beta blocker (to protect CNS development)

Maternal Ab disappears within 3 months: self resolves

After 20 wks gestation fundal height (uterine size) in cm should directly correlate to gestational age in wks +/- 2/3cm

Oligohydramnios: amniotic fluid Index (AFI) <5cm

Abruptio placenta; Uteroplacental Insufficiency

NSAIDs: Decrease PG and leads to fetal vasoconstriction (eg prem closure of PDA)

Decreased fetal renal perfusion -> fetal oliguria

Complications: Meconium aspiration; Preterm delivery; Umbilical cord compression

Polyhydramnios: AFI >/= 24CM

Multiple gestation; Congenital infection eg Parvo

Gestational diabetes: neonatal hyperglycaemia—> increase insulin and IGF

Complications: Fetal malposition; Umbilical cord prolapse; Preterm labour; PPOM

Monochorionic gestation: Shared placenta

Intertwin membrane that meets placenta at 90 degree angle: T SIGN -> Risk of TTTS

Dichorionic (fused) gestation: LAMBDA SIGN

Patients at <32 gestation in preterm labour need:

Indomethacin; Bethamethasone; Magnesium sulfate; Penicillin

External cephalic version: >/=37 wks gestation

If breech/transverse

Preeclampsia: Abnorm placentation and spiral artery formation

New onset HTN and proteinuria and/or end-organ damage (severe features) at >20wks gestation

Can present up to 6 wks postpartum

Urine dipstick not reliable so must confirm with urine protein:Cr or a 24hr collection for total urine

Sustained BP >140/90 on 2 occasions/160/110 once w proteinuria

Chronic BP —->> prior to 20 wks: Tx alpha methyl dopa

Gestational HTN —> no U/A changes —>> can progress to pre eclampsia

Cr should be low in pregnancy eg 0.6 so norm Cr is high!

High Risk: Prior preeclampsia

Preexisting condition —->> Chronic HTN; DM; CKD, SLE

Multiple gestation

Low dose aspirin at 12 wks gestation in all high risk pts! Test all high risk: urine protein:Cr or a 24hr collection for total urine

Moderate Risk: Obesity, Adv maternal age, Nulliparity

Can also be a complication of hydatiform mole if <20wks gestation

End Organ Damage: RUQ pain (hepatic swelling) Hyperreflexia eg clonus, enlarged uterus (pelvic mass); stroke —> focal neuro deficits

Tx: IV Mg sulfate/diazepam prophylaxis and labetalol/methyldopa/hydralazine; delivery at 37 wks

Preeclampsia with severe features —-> delivery >34wks via Induction (if mum n baby stable w/o CI)

C Section indicated: obstetrical indications (failed induction); fetal HR abnormalities Baby >5000g/4500 if gestational diabetes

HELLP Syndrome: Hemolysis, elevated liver enzymes, low platelets

Life threatening; occurs >27 wks

May be severe type of preeclampsia: Can show HTN and proteinuria

D/t abnorm placentation triggering systemic inflamm and activation of coagulation cascade

MAHA is particularly detrimental to liver -> LFTs, liver swelling and distension of Glisson capsule

MAHA -> increased indirect bilirubin production and schistocytes

Hemolysis —> high LDH

Tx: Delivery (warranted at 34 wks or deteriorating maternal/fetal status), magnesium, antihypertensives

IV Fluids and steroids

Magnesium toxicity —-> Decreased DTRs ——>> Tx: Calcium Gluconate Resp depression most concerning sign

Magnesium tx can cause somnolence, flushing, fatigue and nausea but do not signify toxicity Renally cleared!

Intrahepatic cholestasis of pregnancy: Generalised pruritus

Develops in third trimester

Pruritus worse on hands and feet -> No rash

RUQ pain -> Increased bile acids and transaminases (not ALK phos necessarily)

Increased total and direct bilirubin

Complications:

Intrauterine demise, preterm delivery, meconium stained amniotic fluid, neonatal RDS

Management: Deliver at 37 wks, ursodeoxycholic acid, antihistamines

Frequent antepartum monitoring (NST)

Acute fatty liver of pregnancy

Microvesicular fatty infiltrate secondary to mitochondrial dysfunction of fatty acid beta-oxidation

RUQ pain, mildly elevated transaminases and resultant intrauterine demise

Fulminant liver failure: scleral icterus, encephalopathy

——-> manifests as profound hypoglycaemia, Hyperbilirubinameia

Platelets </= 100,000; poss DIC; INR increased etc

Tx: Immediate delivery

Macrovesicular steatosis is typically caused by alcohol, diabetes, or obesity.

Maternal fever d/t intraamniotic infection (IAI) -> fetal tachycardia (>160 bpm)

IAI d/t polymicrobial vaginal bacteria ascending

Maternal fever of >/= 39 Celsius, leukocytosis and/or purulent amniotic fluid

Tx: delivery to prevent fetal morbidity and death

NB: tachy also caused by medications (beta agonists) and fetal hyperthyroidism

Erythroblastosis fetalis

ABO Incombatabilty: More common, less severe

Mother group O, baby A or B

First pregnancy can be affected as no sensitisation needed

Hepatosplenomegaly less common

Weakly positive direct Coombs (fetal RBCs)

Spherocytes

Rh Incompatability

First pregnancy is safe (needs sensitisation)

Hepatosplenomegaly (as more severe)

Unconj hyperbilirubinaemia, jaundice, hemolytic anemia, kernicterus, increased retic etc

Both direct and indirect Coombs strongly +

No spherocytes (totally consumed by macrophages)

RhoD IgG normally given at 28 wks and within 72 hrs

Other indications:

ECV: Think of this as controlled maternal abdo trauma

Induced/spontaneous abortion/evac of molar preg; ectopic preg; CVS; Amniocentesis

Placental abruption/maternal abdo trauma

All pregnant F who are Rh negative with vaginal bleeding to be given Rhogam to decrease risk of

Rh sensitisation

Kell typing: Kell Ag system: group of Ags on RBCs (helps determine blood type)

Anti Kell Abs (IgG)——> transplacental hemolytic disease of newborn

If mother tests positive for anti-K father must be tested to determine risk of fetal K Ag

Implantation bleeding normal in v early pregnancy

PPROM: Rupture of membranes w/o onset of labour

Ferning and positive nitrazine test

External Cephalic Version: Indicated for breech/transverse presentation at 37 wks or over

CI -> CI to vaginal delivery

—->> Prior classical C Section (horizontal)

Prior extensive uterine myomectomy

Placenta previa

Complications: Abruptio placentae; Intrauterine fetal demise

Vaginal delivery

CI if incomplete or footling breech —->> eg unengaged fetal presenting part

——-> Risk of head entrapment

Internal podalic version

Facilitates vaginal delivery’s of second twin by grasping feet and performing breech extraction

Primary Dysmenorrhea

Can be accompanied by n/v and diarrhoea, headaches or back pain

Often established once ovulation cycles start (several years post menarche)

Menopause

Premature if <40

Need 12 months no bleeding to dx menopause -> clinical dx

Give estrogen creams or pesary for dryness, pain and dryness related bleeding, local tx

Prolapse can occur post menopause, tx with hysterectomy

Bladder tape for stress incontinence

Hot flashes d/t declining E2

Menopause and thyroid disorders can present w overlapping sx Hot flashes; insomnia; irreg menses —> both common in F 40-50 -> evaluate TSH and FSH

Dx can be clinical if >45 w 12 month hx of Amenorrhea and no poss physiological cause (eg thyroid)

HRT

Treats vasomotor sx; mood and dryness in F < 60

Alt if CI: paroxetine, SSNRIs; clonidine; gabapentin

CI in liver disease (estrogen metab); breast pain and hypercoag states

Topical estrogen used if mainly vaginal sx

HRT for 5-10 years of surgical menopause

Genitourinary syndrome of menopause

Urinary incontinence, recurrent UTIs

Narrowed introitus; Loss of labial volume

Low oestrogen—-> reduced blood flow and decreased collagen and glycogen production

Reduced glycogen means reduction in normal vaginal lactobacillus activity —-> pH >5

Tx: Vaginal moisturiser and lubricant; Topical vaginal oestrogen

Vesicovaginal Fistula

D/t excessive fetal head compression during obstructed labour (prolonged)

Continuous clear vaginal discharge

Urine increases vaginal pH

May be malodorous d/t surrounding necrotic tissue

Vaginal pooling of urine or area of raised, red granulation tissue

Bladder dye testing used to confirm Dx

(Vulvar) Lichen Sclerosus:

Hypoestrogenic populations eg premenarche or post menopause

Lichenification of perianal area can cause fissures

Vulvar pruritus

Hypopigmented (white) labial lesions

Dx: Clinical w punch biopsy to confirm + rule out vulvar cancer

Tx: Superpotent topical corticosteroids eg Clobetasol

Lichen Planus presents similarly but involves VAGINA: discharge

Genital Lichen Planus

5Ps: Pruritic, purple/pink, polygonal, papules & plaques

Vulvar pain/pruritus; Dyspareunia

Serosanguinous vaginal discharge d/t acute vaginal inflamm

—-> chronic inflamm can lead to vaginal stenosis

Erosive (mucosal) variant most common: Wickham striae: serpentine appearing white striae bordering glazed, erythematous erosions

Lacelike erosions on gingival and palate

Painful oral ulcers and plaque formations on tongue

Dx: vulvar punch biopsy

Tx: High dose corticosteroids

Lichen Planus

Autoimmune disorder driven by CD8 cells

M or F

5Ps: Pruritic, purple/pink, polygonal, papules & plaques

Lacy white network of lines (Wickham striae)

Locations: Skin (ankles/wrists)

Oral mucosa ===> burning sensation in cheeks

Genitalia

Associations: Hep C; ACEIs and thiazides

Lichen Simplex Chronicus

Secondary to repetitive scratching

Hyperplastic response: Thickened, leathery skin

Labial adhesions: Low estrogen production (postmen or pre menses)

Inflammation (any origin) can contribute

Tx: Topical estrogen if sx

PCOS: LH>FSH: 3:1

D/t to anovulatory cycles they have decreased progesterone secretion

Thus constant, unbalance proliferation of endometrium by estrogen

Increased testosterone

Cyst not true cysts—> Antral follicles that have arrested in development d/t hormonal irregularities

E2 not functional so no LH Surge (no ovulation)

Dx requires hx of irregular menstrual cycles indicating anovulation *cyst not needed

Tx: weight loss; OCPs for menstrual regulation

Clomiphene citrate (serm)/ Letrozole for ovulation induction

Hyperinsulinaemia—> exacerbates ovarian hyperandrogenism

—> decreased SHBG and increased sterioidegenesis

Ovarian hyperthecosis

Similar to PCOS but virilisation far worse

Mainly postmenopausal; F

Primary dysmenorrhea: Physiological

Mittelschmerz: Ovulation causes pain mid cycle d/t follicle rupture

Check day 21 progesterone level (mid luteal) to check ovulation

Secondary dysmenorrhea: Pathological

Sx onset >25yrs

Unilateral (nonmidline) pelvic pain; No systemic sx during menses; AUB

Secondary Amenorrhea: MCC is pregnancy

Work up: Pregnancy test ==> Serum FSH/TSH/Prolactin

Functional hypothalamic Amenorrhea: Hypogonadotrophic hypogonadism. Excessive physical training/dieting/stress + depression

Low progesterone w norm estrogen (anovulation)

Ectopic Pregnancy

Most common site is FT (tubal pregnancy), ampulla most common site

Implantation in uterine Cornu counts as ectopic as not Fundus

RFs: PID, smoking, presence of IUD; scar/adhesions; endometriosis

No chorionic villi

Trophoblast invades bvs causing local hemorrhage

Amenorrhea; Syncope; Intraabdo bleeding d/t ruptured ectopic

Adnexal and/or cervical motion tenderness common

Unilateral, most often unilateral adnexal fullness

Guarding with decreased bowel sounds -> rupture

Softening and slight increase in size, typical changes of pregnancy

Beta hCG, serum or urine: Quantitative, in conjunction with TVUS

—-> Inappropriate rise in beta hCG points to ectopic

Progesterone level <5ng/mL 100% specific

Dx: TVUS: Ectopic may be too small to dx via US -> Use serial beta hCGs

Normal intrauterine sac is regular and has echolucent area:

-> double ring/double decidual sign -> represents chorion + decidua

Pseudogestational sac is small and irregular and d/t sloughing of decidua

Laparotomy in hemodynamically unstable with presumed ectopic

Tx: Expectant Management

If asymptomatic with low beta hCG that is declining (spontaneous resolution)

Medical management: Methotrexate. (Toxic to hepatocytes and cleared via kidneys)

CI: presence of gestational sac/embryonic cardiac motion -> Failure of tx likely

Blood dyscrasias, active GI or resp disease

Surgical Management: laparoscopy: salpingostomy/salpingectomy

Evidence of tubal rupture (hemoinstability etc)/CI to medical method

Rh(D) Ig if Rh negative mother

Beta hCG rises more slowly than expected or decline more slowly than abortion Beta hcg <1500 won’t show on US — rise every 2 days

Exposure to teratogens

Viruses (rubella, CMV, Cong Lymphocytic Choriomeningitis virus)

Hyperthermia, radiation

Mercury, alcohol

Inhibitors of RAAS, isotretinoin, warfarin, valproate acid, carbamazepine

Fetal development most vulnerable during organogenesis: 2-8 wks postconception

Ruptured ovarian cyst: Norm benign w minimal free fluid

If pt on anticoag —> hemoperitoneum w instability poss

Peritoneal signs and referred pain to shoulder

Amnioinfusion CI if hx of uterine surgery

Recurrent Pregnancy Loss: 3 or more consecutive losses before 20 wks

Genetic Factors

Maternal/paternal karyotype abnormalities and recurrent aneuploidy (normal karyotyope couple)

Balanced translocations most common

Trisomies, frequency increases with maternal age

Uterine and Cervical Abnormalities

Congenital uterine anomalies

Cervical insufficiency

Submucosal fibroids and endometrial polyps (structural defects)

Malformations d/t DES exposure in utero

Asherman’s syndrome

Uterine septum most common uterine malformation: first trimester losses

Likely d/t implantation failure on avascular septum

Other mullerian fusion abnormalities (bicornuate etc) cause second trimester loss/preterm labour

As do DES exposure anomalies eg T shaped uterus

Dx with Hysterosalpingogram/MRI for malformations

Structural defects interfere other than uterine septum/bicornuate

Dx via TVUS

Cervical insufficiency Dx: TVUS

Painless cervical shortening or dilation in second/third trimester resulting in preterm birth

Associated with congenital uterine anomalies and DES —>> increased vaginal discharge (loss of mucus plug)

Light vaginal bleeding d/t cervical stretching

Pelvic P d/t fetal parts distending upper vagina (can be seen on exam)

Procedures to tx cervical dysplasia such as conisation appear to increase risk

Short cervix: <2 cm w/o hx preterm labour or <2.5 w hx

—-> vaginal progesterone —>> IM progesterone +/- cerclage

Cervical rescue cerclage recommended between wks 13-16

Pts with bulging/prolapse great amniotic sac cerclage CI d/t risk of rupture ———> delivery

Endocrine Factors

Thyroid disorders, luteal phase defect (progesterone insufficiency), hyperprolactinaemia and DM

Hyperprolactinaemia competes with HPA causing:

Insufficient folliculogenesis, oocyte maturation and/or LPD

Tx with dopamine agonist

Infection: Toxoplasmosis, Listeria, HSV, CMV all associated

Listeria: Febrile, gastroenteritis in healthy host (fever, V/D)

Invasive disease in immunocompromised

Immunological Factors

Antiphospholipid syndrome: Abs inc lupus anticoagulant, anticardiolipin, beta-2-GP 1

Venous (majority) and arterial thrombosis, risk increases in pregnancy

Tx: aspirin with or w/o heparin (LMWH)

SLE

Natural Killer cells (associated with preeclampsia and endometriosis also)

Tx: prednisolone

Septic Abortion

Infection norm starts with endometritis involving endometrium and any retained products of conception

Fevers, chills, Abdo pain, vaginal bleeding and malodorous discharge

Pathogens norm those of norm vaginal flora as well as STI

Before D&C STI screening must be done so as not to introduce ascending infection

Tx for both aerobic and anaerobic bacteria and D&C for retained products

Postpartum Endometritis (infection of decidua)

RF: C Section; prolonged ROM (>18hrs) and GBS infection; operative vaginal delivery; chorioamnionitis

Fever >24hr postpartum —> Most common etiology for postpartum fever is endometritis Uterine fundal tenderness (not suprapubic) and purulent lochia (not always present)

D/t direct inoculation of uterus by vaginal Flora

Tx: IV broad Spec Abs: Gentamicin and Clindamycin w or w/o ampicillin

Septic Pelvic Thrombophlebitis

RF: C Section; pelvic surgery; endometritis; PID; Pregnancy (postpartum); malignancy

Pathophysiology: Hypercoagulability; Pelvic venous stasis & dilation; Vascular trauma; Infection

==> pregnancy is a hypercoagulable state

Persistent Fever unresponsive to Abs (>48hrs postpartum)

No localising sx/signs w Negative infectious evaluation

Dx of exclusion

Tx: Anticoagulation and Broad spectrum Abs

STD Assessment

Syphilis screen: Penicillin crosses placenta so can treat foetus as well

Chlamydia: Screening with DNA probe

Gonorrhea: Ceftriaxone with azithromycin for penicillin resistant strainstx chlamydia

Hx of HSV should receive prophylactic acyclovir/valcyclovir at 36 wks

If no current active infection then vaginal delivery safe

Vertical transmission: Meningoenceph/sepsis w LT sequelae: Blindness, neurocog disability, persistent seizure

HIV: Caesarean only if viral load high ie >1000

GBS: Rectovaginal culture at 36-38wks

Intrapartum IV penicillin G prophylaxis (IAP):

If GBS+ culture

Hx of GBS Bacteriuria/UTI (regardless of tx)

Unknown status/fever/>18hr ROM

Prior infection with early onset neonatal GBS infection

Not indicated for planned C Section w/o labour/ROM as baby does not enter birth canal

Alt: IV Clindamycin/Erythromycin

Tdap (inactivated as reduced) Vaccine at 27-36 wks —> Tri3 use protects mum against pertussis and gives baby passive immunity —> in every pregnancy regardless of vaccination hx

Women who did not receive vaccine during pregnancy should be given immediately postpartum

Inactivated influenza as soon as it becomes available during pregnancy

Neonatal VZV Infection

Systemic involvement: pneu, hepatitis, menigoencephalitis

Tx: Acyclovir

Prevention: Administer VZV Ig if maternal infection develops 5 days before to 2 days postpartum

—-> same if immunocompromised/pregnant etc (no live vaccine)

PEP in non neonate and immunocompetent person

—> Varicella Vaccine Alone (no need fo VZ Ig) if not fully immunised

Infants < 1 year outside neonatal period at lower risk ==> no vaccine or VZ Ig

First Prenatal Visit

STD Screen HBsAg and rubella titre

Depression and lifestyle: alcohol etc

Gestational DM if high risk —> 2nd Tri for everyone else (24-28wks)

TSH

Screening

Urine culture (screening for UTI) in first Trimester only: Wks 12-16 Hepatitis C (only screen high risk):

Management: Ribavirin is teratogenic so avoid

Hep A & B Vaccination (killed vaccines)

Vertical transmission strongly associated with maternal viral load (C Section not protective)

Breastfeeding encouraged unless nipple injury (bleeding)

CI vaccines in pregnancy: HPV; MMR; Live Influenza; Varicella (can give VZV Ig)

Recommended vaccinations during pregnancy for high risk patients (multiple STDs)

Hep B and A, Pneumococcus, Haemophilius Influenza, Menigococcus, VZV Ig

Negative Hep B surface Ag Assay signifies zero Hep B exposure ——->>> vaccinate!

Rubella

Unvaccinated mother: Have vaccine and wait 1 month before conception

Rubella can cause miscarriage

Tubo Ovarian Abscess

Complication of PID -> Hospitalisation and IV Abs

Candida: vulvovaginal candidiasis

Itchy vulva—-> excoriation—-> dysuria -> pH 4-4.5 (normal range)

Discharge, if present —> thick, cottage cheese like

Abs such as tetracycline/Clindamycin increases risk

Tx: Fluconazole/miconazole

Trichomoniasis

Positive whiff test

Friable erythematous cervix with punctuations —> Strawberry Cervix

Thin, green/yellow copious discharge/ watery -> do wet mount to differentiate BV

Vaginal pH 5-6.0

Wet prep —>> motile, flagellated, pear shaped trichomonads

Tx: Metronidazole

Bacterial Vaginosis

Gardnerella vaginalis: Gram variable staining

Positive whiff test + Elevated vaginal pH

Turbid discharge: thin, gray and coats vaginal walls; No erythema

Positive nitrazine test —> Clue cells on wet prep

Tx: Clindamycin

Acute Cervicitis: Cervical motion tenderness absent! Postcoital bleeding -> Friable cervix (bleeds easily)

Thick mucopurulent discharge

Poss dysuria, dyspareunia and pruritus

Fever and abdo pain unusual ——->> raises concern for PID Chlamydia or Gonorrhea usually -> Confirm Dx with NAAT

Tx with azithromycin and ceftriaxone

Complication: Preterm birth in future pregnancy

Pelvic Inflammatory Disease

Constant Pelvic pain, tenderness of cervix (worsens with menses) OR adnexa

Intermenstrual spotting d/t cervicitis (friable)—-> Abnormal VAGINAL BLEEDING Can manifest as new bleeding in previous amennorheic pt

Cervical motion tenderness

Purulent discharge

Complications: Tubo-ovarian abscess; Infertility; Ectopic Pregnancy, Perihepatitis

Tx: IM Ceftriaxone + ORAL doxycycline/Azithromycin if outpatient

Inpatient: Severe vomiting; hx of noncompliance; unstable vitals; pregnant

Perihepatitis or tubo-ovarian abscess; failed outpat tx Tx: IV Cefoxitin/cefotetan + oral doxy/IV Clindamycin + gentamicin if inpatient

Abortion:

Spontaneous Abortion most common complication of pregnancy

Defined as <20 wks and <500g

Threatened Abortion is arising from within uterus that occurs before completion of 20th wk

First Trimester vaginal bleeding (could be implantation bleeding -> benign)

No passage of products of conception

No cervical dilatation

Can resolve

Management: Outpatient observation and serial USs

Complete Abortion is expulsion of all products of conception before wk 20

Incomplete Abortion is expulsion of only some of the products of conception

Inevitable Abortion refers to bleeding within the uterus prior to wk 20

With dilatation of cervix

No passage of products of conception; No cardiac activity

Missed Abortion is nonviable pregnancy that has been retained in uterus

No cervical dilatation

No expulsion of products of conception

Foetus present but No cardiac activity

Septic Abortion, embryonic/fetal demise has occurred and intrauterine infection has developed

Infection has potential to spread systemically

Most commonly d/t DIY abortion

Tx for non viable spontaneous abortions: Misoprostol and suction curettage (if unstable)

Misoprostol (PG E1 analogue) induces contractions and expulsion of products

—-> only if hemostabile

CT

CM

CC

Dark blood -> clot

If beta hCG levels start rising post abortion, plateau or are persistent >6 months

Malignant postmolar gestational trophoblastic disease

Complications of Abortion: Bleeding that may be life threatening

Infection, intrauterine adhesions (Asherman) and infertility

Aneuploidy (abnorm chromosome number) is most common genetic abnormality

Turner’s syndrome is the single most common aneuploidy

Trisomy 16 is the most common trisomy resulting in abortion

Genital tract structural changes seen in women whose mothers took Diethylstilbestrol (DES)

Acquired anomalies: Fibroids (esp submucosal) and endometrial polyps

Asherman’s Syndrome: Synechiae within uterine cavity -> Infertility/ recurrent miscarriage

Most commonly d/t D&C

Anembryonic Pregnancy (Blighted Ovum)

Embryo fails to develop or is resorped after loss of viability

Cervix closed

Falling or abnormally rising levels of beta hCG are dx of an abnormal pregnancy

Heterotopic Pregnancy: Normal implantation + ectopic

Hydatiform Mole: Beta hcg >100 000

Theca lutein cysts present in 50% of cases

Bilateral, large, multi septated ovarian cysts

Caused by excessive beta hCG production ——-> ovarian hyperstimulation

Higher incidence in Eastern countrie; blood group A

Uterus may be abnormally large and contain heterogenous cystic mass

Heavy vaginal bleeding d/t passage of hydronic villi (heterogenous cystic mass)

Overt hyperthyroidism (d/t beta hCG); hyperemesis gravidarum

Preeclampsia w severe features

Classically described as Swiss cheese or Snowstorm pattern on US

Early molar pregnancy can present as anembryonic gestation or spontaneous abortion

Preeclampsia at <20 wks d/t abnorm placental spiral A development

Only partial moles contains fetal parts RF: Vit A Deficiency (Roux-en-Y) and adv maternal age

Management: D&C; Serial serum beta hCG post evac (can take 8wks to become undetectable);

Contraception for 6 months

If beta hcg >40,000 prophylactic chemo needed

Avoid pregnancy for a year and avoid IUD/IUS (intrauterine devices/system)

SLE Nephritis in pregnancy

Preterm birth, C Section, Preeclampsia; Fetal growth restriction; Fetal demise

Constitutional small Infant: Genetically predisposed small infant

Association: Short mother; low prepregnancy weight; Asian; F infant

Antepartum course

Estimated fetal weight <10% for gestational age (but not d/t growth restriction)

———> norm umbilical A Doppler and appropriate interval growth

Outcomes: No LT issues

IUGR

Estimated fetal weight <tenth percentile for gestational age

Symmetric: Global growth delay

Onset in Tri1

D/t chromosomal abnormalities or congenital infection

Asymmetric: Head sparing growth delay

Onset Tri2/3

D/t uteroplacental insufficency; maternal malnutrition

Management of both: Weekly biophysical profiles; serial umbilical A Doppler; serial growth US

Twin-twin transfusion syndrome

Unique to monochorionic, diamniotic twins which share one placenta and have separate amniotic sacs

Earliest finding on US is oligohydramnios (<2cm) in 1 twin and polyhydramnios (>8cm) in other

Tocolytics: At 34 wks + —> delivery

Indomethacin: First line <32 wks

Side effects: Maternal: Gastritis and Plt Dysfunction

Fetal: Oligohydramnios and closure of ductus arteriosus

Nifedipine

First line 32-34 wks

Side effects (d/t periph vasodilation): Maternal: Tachycardia/palpitations; nausea; flushing; headache

Terbutaline/Ritodrine (beta agonist)

Short term tocolytic: inpatient use. (Black box side effect profile)

Side effects: Maternal: Tachycardia/arrthymias; hypotension; hyperglycaemia; pulm oedema

Used to relax uterus when there are contractile abnormalities causing fetal HR abnormalities

——> tachysystole (>5 contractions in 10 min) or tetanic contractions (contractions lasting >2 min)

Magnesium sulfate is a weak tocolytic

Preterm Labour Mangement

34-37wks: Pen if GBS +/unknown +/- bethamethasone

32-34 wks: Pen if GBS +/unknown + bethamethasone

Tocolytics

<32 wks: Pen if GBS +/unknown + bethamethasone

Tocolytics

Magnesium sulfate

Tocolytics CI if ROM as contractions indicate a problem that requires delivery/intervention

Abdo myomectomy w/o uterine cavity entry —->> vaginal labour fine

Abdo myomectomy with uterine cavity entry (eg Fibroid removal)

—->> vaginal labour CI: C Section at 36-37wks

Previous classical C Section (vertical incision)

—->> vaginal labour CI: C Section at 36-37wks

If either presents in active labour—-> urgent laparotomy and C Section

Postpartum hemorrhage

500ml post vaginal delivery or >1000ml post caesarean

Can cause haemorrhagic shock

Uterotonics: oxytocin, methylergonovine (CI in HTN), carboprost (PGF2alpha CI in PID and asthma),

misoprostol

Intrauterine balloon tamponade

Uterine artery embolisation (can affect implantation in next pregnancy)

Hysterectomy

Uterine Atony: MCC of PPH Uterus fails to contract and is soft (boggy) and enlarged (eg above umbilicus) on physical examination

Fundal height of over 2cm postpartum indicates boggy uterus

D/t fatigue (eg prolonged labour), over distension

RF: forceps assisted and hypertensive disorders; Chorioamnionitis

Tx: Bimanual uterine massage; uretotonic meds

Retained products of conception

RF: Succenturiate placenta; Manual extraction of placenta;

Hx of prev uterine surgery/retained placenta

Placenta accreta or placental detachment failure

Enlarged, boggy uterus; placenta missing cotyledons; retained fragments on US

—> retained placenta if failure to deliver placenta within 30 min of fetal delivery

Complication: endometritis

Tx: Manual extraction; D&C

Genital tract trauma

RF: Operative vaginal delivery

Laceration of cervix/vagina; enlarging hematoma

Tx: Laceration Repair

Inherited coagulopathy

RF: Hx of abnorm bleeding in pt/family

Continued bleeding despite contracted uterus

Tx: Correct coagulation

Post C Section: injury to uterine artery

===>> retroperitoneal hematoma (rare and life threatening cause)

—> no incisional bleeding and min abdo/back pain

Indications for operative vaginal delivery

Maternal exhaustion, fetal distress

Maternal conditions where Valsalva CI: HOCM etc

100% dilation needed

C Section more risky for mother cf vaginal delivery

——> in breech ECV used as vaginal delivery of living neonate has risk of trauma/hypoxia

———-> not indicated for IUFD and delivery

FHR Trace

Category III —-> absent variability

IV resuscitation interventions (O2; fluids; cease uretotonic S)

Repositioning

Pts remote from delivery (dilation) —> emergency C Section

ANTENATAL CARE:

Post 36 weeks aspirin tx is stopped as this could cause early closure of PDA

Inherited thrombophilia increases risk of thrombi postpartum not during pregnancy

Succenturiate Placental Lobe

Accessory lobe

Non tapering vessel extending to margin of membranes

Commonly torn from primary lobe in Delivery

Postpartum bleeding!

Screening

Aneuploidy screening using Cell free DNA at 10 wks

Chorionic Villus Sampling: 10-13 wks, invasive

Dx for aneuploidy but not neural tube defects (AFP in amniotic fluid)

Amniocentesis: 15-20 wks

Dx aneuploidy and neural tube defects

Nonstress Test (NST): Decreased fetal movement: Assess with NST

Fetal movements associated with accelerations of HR

—-> Hypoxic and acidotic foetuses move less so non reactive NST can signify this

2 or more Fetal HR accelerations, at least 15 bpm above baseline and lasting min 15s

REASSURING (reactive)

Non reactive: most commonly d/t quiet fetal sleep cycle (</= equal to 40min)

Fetal hypoxaemia and acidaemia

Fetal HR accelerations require mature sym NS which occurs around 28wks gestation

Biophysical Profile

5 components: NST w US evaluation of:

—>>> fetal breathing movements, fetal movement, fetal tone and amniotic fluid vol

Non reactive NST requires full biophysical profile or contraction stress test

————> high false positive rate (ie non reactive does not = acidaemia)

Contraction Stress Test equivalent to Biophysical profile in assessing fetal status

—-> Oxytocin/nipple stimulation used until 3 contractions every 10 min occurs

—-> CI: CI to labour (eg placenta previa, prior myomectomy etc)

Biophysical Profile components: Continuous observation for 30 minutes

NORM FINDING: >4

NST. Reactive fetal HR monitoring

Amniotic Fluid Vol. Single deepest fluid pocket >2 x 1cm or amniotic fluid index >5

Fetal Movements. >3

Fetal tone. >1 episode of flexion/extension of limbs or spine

Fetal breathing. >1 breathing episode for >30 sec

Movements

Maximum score of 10

0=abnormal; 2= normal per component

Polyhydramnios does not affect Biophysical Profile

Modified Biophysical Profile

Combines NST with Amniotic Fluid Index

Preterm labour

Strongest risk factor is previous preterm labour

Multiple gestation

Low BMI/Inadequate weight gain

Hx of cervical surgery inc conisation

Evaluate risk: TVUS to measure cervical length in second trimester

Gestational diabetes

One hr real glucose tolerance test (24-28 wks) >140 screening test

Dx confirmed with 3hr oral glucose tolerance test >155

Tx: Diet; Metformin/insulin

Multiple Gestation

Maternal complications: Iron deficiency anaemia; Hyperemesis Gravidarum

Fetal Complications: Growth restriction; Malpresentation (breech); Preterm delivery

Asymptomatic Bacteriuria (UTI)

Pregnant F have increase risk of pyelonephritis and complications (preterm delivery/LBW)

Tx: Cephalexin; AmoxiClav; Nitrofurantoin; Fosfomycin

Trimethoprim: neural tube defects in Tri1 and kernicterus risk Tri3

Safe in Tri2

Do repeat culture (test of cure) a few wks after completion of antibiotics

Persistent Bacteriuria/failure to respond —> daily Abs

Acute pyelonephritis

RF: Asymptomatic Bacteriuria; DM; Age <20

High risk of sepsis

Pathogens: E Coli; Klebsiella; Enterbacter; GBS

Complications: Low birth weight; ARDS

Retroperitioneal irritation can irritate uterus (non painful contractions) or preterm labour

Tx: IV Abs until afebrile and Supportive; AmoxiClav

Aminoglycosides cause ototoxicity in baby

Perineum: Lasts 6-8 weeks (postpartum period)

Normal postpartum discharge

Lochia rubra (blood, shreds of tissue and decidua)

—-> occasional small clots until 3-4 days postpartum; cervix may be min dilated

Lochia serosa —-> serosanguinous (pink); brownish (old blood)

Lochia alba -> thicker, mucous and yellow-white (WBCs and degenerated decidual cells)

Lochial secretions cease after 5-6 wks

Resumption of postpartum menstruation

If formula feeding: 8-14 wks

If breastfeeding exclusively: > 6 months normal

External cervical os becomes transverse slit post vaginal birth only

Hymen heals as carunculae myrtiformes (fibrosed nodules of mucosa)

Ovulation suppressed d/t high prolactin in non lactating for 3 wks, 6 months for lactating

Polymorphic Eruption of pregnancy: Pruritic erythematous papules in Tri3

Starts within abdominal striae

Spares palms and soles

Oxytocin: Severe hyponatraemia is a side effect —-> similar structure to ADH

Ovulation

Cervical mucus secretion close to ovulation (late follicular stage) increases in quantity

—> discharge: clear, elastic, thin (uncooked egg white)

—-> thickens after ovulation (less hospitable to sperm)

If Corpus Lutein removed before 10 wks gestation (luteal-placental shift)

—->> progesterone supplementation (uterine quiescence)

Cervical mucus plug

Pregnancy -> Barrier to ascending infection

Brown/red/yellowish and thick

Shed before/during labour

Postpartum urinary retention

Inability to void >6hrs after vaginal delivery/catheter removal post C Section

RF: Primiparity; epidural—-> bladder atony; operative vaginal delivery;

Perineal injury —> Pudendal N damage; C Section

Small-volume voids/inability to void; Dribbling urine

Overflow incontinence: Lower abdo P; overdistended bladder

Management: Self limited condition; intermittent catheterisation

HCG

Hormone secreted by syncytiotrophoblast

Responsible for maintaining corpus luteum

Also promotes male sexual differentiation and stimulates maternal thyroid gland

Production begins 8 days post fertilisation, doubles every 48 hrs and peaks at 6-8 wks

Two subunits: alpha and beta -> Alpha common to TSH, LH and FSH

Beta used in pregnancy test

Full term: born at 37 weeks or more

HR should be 100-160 BPM

RR 40-60

Absent red reflex: Congenital cataract, retinoblastoma or glaucoma

Screening:

PKU; Congenital syphilis; Hearing loss; ABO incompatibility via direct Coombs

Congenital hypothyroidism ——> thyroid dysgenesis MCC

->norm at birth as sx arise once maternal T4 wanes

Single umbilical artery: likely other abnormalities esp renal

Hyperemesis Gravidarum

RF: Hydatiform mole; multifetal gestation; Hx of hyperemesis gravidarum

Severe, persistent vomiting

5% loss of prepregnancy weight

Dehydration -> Orthostatic hypotension; Hemoconcentration

Ketonuria

Hypochloraemic metabolic alkalosis -> Hypokalaemia

Tx: Hospitalisation; antiemetics and IV Fluids

Testes

SRY gene (sex determining region of Y chromosome) encodes TDF

TDF initiates chain of events that results in differentiation of gonad into testis

Sertoli cells produce antimullerian hormone (mullerian inhibiting hormone)

————->>>>>> Leydig cells differentiate and produce testosterone

Antimullerian hormone -> regression of paramesonephric ducts (mullerian ducts)

Testosterone influences persistence + differentiation of mesonephric (wolffian) ducts

Genital sex (external) develops d/t absence/presence of androgen

Genital Ducts

Mesonephric Ducts (regress in female mostly)

Differentiate into: Epididymis, Ductus Deferens and Ejaculatory Ducts if Testosterone present

Both: Trigone of Bladder

Female: Gartner’s Cysts

Paramesonephric Ducts

Female -> Regress if MIF present

Fallopian Tubes and Uterus, part of Vagina

Neural Tube Defects (NTDs)

Maternal serum AFP detects open NTDs

Amniotic fluid acetylcholinesterase

Maternal heat exposure in first tri and neural tube defects

Chromosomal Abnormalities

Downs: Low maternal AFP, low E3, high hCG

TRISOMY 18: Low maternal AFP, low E3 and low hCG

TRISOMY 13: High/norm maternal AFP, norm E3 and norm hCG

Klinefelters Syndrome: FSH>LH

Small testes, azoospermia, gynecomastia, infertility

High levels of gonadotropin, FSH up regulates aromatase (increased oestrogen)

Mental retardation

Infertility d/t testicular fibrosis w seminiferous tubule dysgenesis,

Tx: Testosterone

Congenital Adrenal Hyperplasia

Taller than other children but epiphyseal plate closure at age 10

————->short adults (short limbs)

Early pubic hair and acne but puberty never starts -> No menstruation or breasts

High level of adrenal androgens and 17-hydroxyprogesterone (dx test)

Males: Short adults but normal external genitalia

Vomiting, progressive weight loss and dehydration d/t low serum sodium and high potassium

Tx: cortisone

Aldosterone. Testosterone

21 hydroxylase deficiency. 2(down). 1(up)

17 alpha hydroxylase deficiency. 1(up). 7(down)

11 beta hydroxylase deficiency. 1(up). 1(up)

Whenever you have a 1 it goes up, otherwise it goes down!!!!!!!!

All have low cortisol

Other causes of low testosterone: low desmolase, low 3 beta hydroxysteroid

Gestational age: (time elapsed since first day of last menstrual period)

Determined by crown rump length

Cardiac activity discernible at 6 wks; Limb buds 8 wks

Finger and limb movement at 10 wks

Braxton Hick’s are painless contractions

Average cervix length is 3-4cm

Cell free DNA testing can be used after 10 wks for aneuploidy

Quad screen between 15-20 wks

Chorionic villous sampling between 10-13 wks

Amniocentesis between 15-20 wks

Prenatal visits Every 4wks from 0-28 wks gestation

Every 2wks from 28-36wks gestation

Weekly from 36wks gestation

Weight gain of 11.5-16kg expected

Labour: 3-5 contractions in 10 minutes + cervical change

Cervix softens, effaces (shortens+thins) and dilates

With effacement the mucous plug within cervical canal may be released

Passage of small amount blood tinged mucous (bloody show)

3 Stages of Labour

1: Interval from Onset to full cervical dilatation: Latent and Active phases

2: Complete dilatation to delivery

3: Delivery of infant to delivery of Placenta

1: Start of Acute Phase at 6cm dilatation

Arrested labour if cervix dilated 6 or more cms and one of the following:

6 or more hours of inadequate contractions and no cervical change

4 or more hours of adequate contractions and no cervical change

Tx: Operative vaginal delivery/C Section —> oxytocin used for prolonged labour not arrested!

Fetal scalp electrode USED to monitor foetus post rupture of membranes when ext monitor inadequate

——-> maternal obesity etc

Indications for Induction: Preeclampsia, eclampsia, HELLP, diabetes, chronic HTN, heart disease

Late term/post term, fetal abnormality, chorioamnionitis, premature rupture of membranes,

Oligohydramnios, placental insufficiency, suspected growth restriction, fetal demise,

Multiple gestation

Contraindications to Induction:

Contracted pelvis, placenta Previa, vasa previa, transverse lie,

Care taken with breech and prev caesarean with low lying scar

Methods of cervical ripening: Bishops score

Prostaglandin: Misoprostol (PGE1) and Dinoprostone (PGE2); Balloon Catheter

Methods of Labour Induction

Oxytocin; Amniotomy (iatrogenic rupture of membranes)

Cervical changes during labor

—-> softening/ripening

effacement: thinning/shortening of cervix

dilation: widening of cervix

Fetal station: describes position of fetal head relative to maternal ischial spines

-5, -4, -3, -2, -1, 0, +1, +2, +3, +4, +5

-5 = initial position prior to labor

0 = at level of narrowest point of ischial spines

+5 = at vaginal opening

Maternal Physiology during Pregnancy

Cardiovascular System:

Heart size increases; Apical beat shifts laterally

Blood volume expands: Hypervolaemia of Pregnancy

Human chorionic somatomammotropin and progesterone promote erythropoeisis

Cardiac Output increases d/t hormones and AV shunt effect of uteroplacental circulation

Stroke volume and HR increase

BP drops and pulse pressure widens

Renal blood flow increases as does GFR

Systolic ejection murmurs d/t increased output and decreased viscosity

Continuous murmurs at left eternal edge d/t internal thoracic (mammary) artery

Pulmonary System

Elevation of diaphragm causes reduction in TLC and FRC

Increase in tidal volume with norm RR (increased minute ventilation)

Hyperventilation: decreased maternal PC02 with mild alkalosis and increases PO2

Renal System

Kidneys and ureters lengthen and dilate -> Increases risk of ascending UTIs

Increased GFR with saturation of tubular resorption capacity——->>> glycosuria (increased UTIs)

Renin activity increases but pregnant women relatively resistant to pressor effects of ANG II

Increased vasopressin——>> DI like condition

Oestrogen production by placenta stimulates RAAS—-> increases aldosterone

——>> increases renal Na reabsorption and water retention

Bladder -> capacity increases to 1500ml

GI System

Gum hypertrophy, bleed easily (similar occurs with OCP)

Heartburn, decreased oesophageal peristalsis, relaxation of LES

Slowed GB——>>>bile stasis

ALP isoenzymes produced by placenta can double ALP; albumin reduction

Haematology

RBCs

Mass expands but not as much as plasma volume thus physiological anemia of pregnancy

Placenta actively gives foetus iron so this no it anemic even if mother severely anemic

No tx unless Hg <11

Platelets

Pregnancy associated thrombocytopenia d/t increased consumption

Coagulation Factors increase: net procoagulant effect

Skin

Hyperpigmentation: Linea Nigra and Melasma (exacerbated by sun)

Elevated levels of melanocyte stimulating hormone, oestrogen and progesterone

Seen in OCP use too

Striae Gravidarum (hyperaemic skin, stretch marks)

Decreased collagen adhesiveness and increased ground substance formation

Genetic predisposition

Spider angiomas, palmar erythema and cutis marmorata (mottled d/t vasomotor instability)

Worsening varicosities

Compression on vena cava increases venous pressures in legs, anus (hemarrhoids) and vulva

Nails become brittle and show horizontal grooves (Beau’s lines)

Metabolism

Increased LDL and TGs

Human placental lactogen increases insulin resistance

Placenta

Basic parenchyma is the trophoblast

HCG produced by syncytiotrophoblast

Cytotrophoblasts (Langhans cells) divide and proliferate

Syncytiotrophoblast is invading tissue

Placenta is fetal in origin

Cotyledons are subdivisions of placenta, devoid of flow during contractions

Prolonged contractile phase -> uterine tetany can cause fetal hypoxia

Placental Secretions

Human chorionic somatomammotropin/ human placental lactogen

Made by syncytiotrophoblast

Enhances action of GH and decreases effect of insulin in vivo

Oestrogen and progesterone, DHEAS

Estriol -> Increases uteroplacental blood flow

Progesterone maintains myometrium is state of quiescence and blocks immune responses against

foetus

Transfers O2, CO2, Urea, IgGs (pinocytocysis), some viruses (poss pinocytosis)

Lack of transfer: Insulin, Heparin (both too large)

Anatomical Disorders of Placenta

Twin-twin transfusion syndrome

Monochoroidal twins

Twin receiving more blood is plethoras and polycythemic, poss cardiomegaly

Donor twin pale, anemic and reduced organ weight (intrauterine malnutrition)

Chorioangioma of Placenta: Benign neoplasm

Fetoplacental capillaries (hemangioma)

AV shunting -> Hydramnios, hemorrhage, preterm delivery and growth restriction

Amniotic Bands: Constriction, amputation, deformities, syndactyly, clubfoot

Umbilical Cord

Velamentous Insertion: Umbilical vessels divide and course through membranes

Vasa previa: umbilical vessels ahead of foetus

Short cord, no Wharton jelly

Single umbilical Artery

Risks: Age, ethnicity, multiple gestation, fetal sex and smoking

Increases risk of congenital and chromosomal anomalies eg malformations

Hyperandrogenism during Pregnancy

Luteoma: Solid uni/bilateral ovarian masses

—-> Spontaneous regression of masses postpartum

Theca-lutein cyst: Cystic, bilateral ovarian masses

—> Spontaneous regression of masses postpartum

Sertoli-Leydig Tumour: Solid unilateral ovarian mass

—> surgery required Tri2/Postpartum

Management of bilateral, benign masses is observation and expectant management

==> masses usually resolve postpartum d.t declining beta hCG levels

Short interpregnancy interval: <6-18 months from delivery to next pregnancy

Complications:

Maternal anemia; PPROM; Preterm delivery; Low birth weight (growth restriction)

Intraamniotic infection: chorioamnionitis

RFs Prolonged rupture of membranes (>18hrs)

PPROM (nitrazine positive fluid: alkaline amniotic fluid)

Internal fetal/uterine monitoring devices

Repetitive vaginal examinations

Presence of genital tract pathogens

Dx: Maternal fever plus 1 or more of following:

Fetal tachycardia (>160 bpm); Maternal leukocytosis; Purulent amniotic fluid

Management: broad spec Abs and Delivery (Labour Augmenation)

Complications: Postpartum haemorrhage; endometritis

Fetal: Preterm birth; pneumonia; encephalopathy

Uterine tachysystole: >5 contractions/10min

D/t uterotonic is agents eg oxytocin

Contractions temp interrupt inter villous blood flow

Recurrent Late Decelerations (in >/=50% of contractions)

Moulding (change in fetal skull shape d/t maternal expulsion efforts) and captured (scalp edema d/t

prolonged pressure) d/t cephalopelvic disproportion

Premature Prelabour rupture of membranes (PPROM)

Membrane rupture <37 wks prior to onset of labour: >1hr before onset of labour

Risks: Prior PPROM; Genitourinary infection (esp BV); BMI <19.8; Cervical insufficiency

Dx: Vaginal pooling/fluid from cervix

Nitrazine-positive (blue) fluid -> Ferning on microscopy

Common complications: Placental Abruption

Decreased amniotic fluid volumes leads to uterine decompression:

—>>> Bleeding and separation of placenta from uterus

Additional complications: Intraamniotic infection, preterm labour, umbilical cord prolapse

Management: <34wks: Latency antibiotics (ampicillin+azithromycin; prolong pregnancy)

34 wks/Comp: Delivery, antibiotics, steroids and Mg if <32wks

Preterm Labour (<34 wks) Dx: Regular contractions w cervical change —> Preterm Labour

—> w/o cervical change test FFN (High PPV and NPV)

Fetal Fibronectin (FFN) (choriodecidual interface) leaks into vagina if preterm delivery likely in next wk

—>> Sampling at 24-34 wks

Vaginal bleeding can give false positive

Endometrial Hyperplasia: Increase in endometrial thickness

D/t unopposed oestrogen

TVUS: If endometrium thickened——>biopsy

Tx: Mirena

Ablation of functional endometrium

Malignant Tumours: Spread by blood!!!!

Endometrial carcinoma

Choriocarcinoma

Usually disease of post menopausal women:

3mm thick endometrium

Postmenopausal bleeding (most common cause of this is HRT!)

In pre menopausal women: >5mm thick endometrium + AUB

Risk factors: unopposed oestrogen (see ovarian)

Pelvic irradiation (triggers ovary—-> increases oestrogen); DM

Functioning ovarian tumour

Tamoxifen

Family hx of breast, ovary or colon cancer

Tobacco is protective: stimulates estrogen metabolism in liver so decreases serum levels

Dx: Biopsy gold standard

Tx: Stages 1/2: Total Abdo hysterectomy with or w/o oopherectomy and/or radiation

Extension beyond uterus and cervix: radiotherapy/chemo post surgery

Abnormal Uterine Bleeding: PALM-COEIN Commonly d/t uncontrolled endometrial proliferation (d/t unregulated excess oestrogen)

Structural: PALM

Polyps

Adenomyosis

Leiomyoma

Malignancy

Non Structural: COEIN

Coagulopathy

Ovulatory Dysfunction

Endometrial

Iatrogenic

Not yet classified

In F <45 with AUB the absolute risk on endometrial cancer low

===> start on combo pill w/o endometrial evaluation (medical management)

=====> if medical management fails or indication of Lynch Syndrome ===> Endometrial biopsy!!!!!

Cervical Ectropion

Cells from the inside of the cervical canal are present on the outside of the vaginal portion of the cervix.

D/t hormonal changes (young F); OCPs and pregnancy

Can cause postcoital and intermenstrual bleeding, excessive, non purulent discharge and bleeding

post pelvic exam

Postmenopausal bleeding workup

Always do endometrial biopsy OR TVUS of endometrium

—>> TVUS shows thickness of endometrial stripe

Pelvic Organ Prolapse

Cystocele; Rectocele; Enterocele (SI); Procidentia; Apical prolapse (uterus, vaginal vault)

Management: Weight Loss; Pelvic Floor exercises; Vaginal Pessary; Surgery (if good candidate)

Sarcoma Botryroides

Eg embryonal rhabdomyosarcoma

Presents in infancy and early childhood

Non friable nodules protruding from vagina resembling cluster of grapes

Choriocarcinoma: Gestational trophoblastic neoplasia

RF: Adv maternal age; prior complete hydatiform mole

MC occurs after molar pregnancy but can occur after any type of preg inc abortion

Amenorrhea/AUB; Pelvic P/pain

Sx d/t metastases (lung, vagina)

—-> bloody, purulent discharge; red vascular friable nodules/lesions

Uterine mass; symmetrically enlarged mobile uterus

Elevated beta hCG

Tx: Chemo

Cervical cancer

Smear first as disturbs cells -> Swap second as only need mucous/fluid

Squamous cell carcinoma or adenocarcinoma

Columnar epithelium undergoes immature squamous metaplasia–> mature squamous metaplasia

NORMAL!!!

Infection with HPV——> immature squamous metaplasia—-> dysplastic squamous epithelium

HPV 16 and 18 most common in UK to cause cervical cancer

HPV 6 and 11 do not cause cancer, cause warts

As tumour extends laterally through parametrium and pelvis (low back pain)

—-> obstruction of lymphatic (lymphedmea) and ureters (hydronephrosis)

Cervical cancer spreads via lymphatics!!!!

Risk Factors:

Early sexual intercourse; Multiple partners; Hx of STDs (inflamm)

Multiparity (inflamm, stress on epi)

Immunodeficiency

LT oral contraceptive use (>5 years): combined pill causes ectropion of transformation zone

Smoking

Sx: Post coital bleeding

Bleeding on touch (ie during smear)

Smelly vaginal discharge

Growth seen on cervix

AIDS defining illness in HIV positive

Inguinal LAD

Cervical intraepithelial neoplasia (CIN)

Preinvasive Carcinoma:

CIN1: Immature cells in lower 1/3 of epithelium

CIN2: immature cells in lower 2/3 of epithelium

CIN3: Immature cells extending beyond lower 2/3 epithelium

CIS: Full thickness immaturity of epithelium

Invasive Carcinoma

Biopsy confirms dysplasia (colposcopy)

Squamous cell proliferation resembles cauliflower

Prevention: HPV vaccine

Quadrivalent (Gardasil): 16, 18, 6 and 11

Bivalent (Cervarix): 16 and 18

Vaccination for boys to prevent anal cancer

Gardasil: Highly purified virus like particles of L1 protein of HPVs

Post menopausal, squamocolumnar junction higher up

Biggest issue with smear is inadequate sample

Must wait 6 months to redo for cell regrowth

Smear: Every 3 years ages 21-65 years

Ages 21-29 PAP smear only

HPV Vaccination w/o HPV testing in unvaccinated F/M age 11-26 routine (can give ages 9-45)

———> NOT indicated in pregnant F

Over 30yrs requires HPV cotesting

Squamous cells brown, columnar blue

Koilocytosis: halo cells seen post HPV: Lots of blue!

Abnormal smear: High nuclear:cytoplasm ratio, nuclear pleoimorphism,

hyperchromasia of nucleus (Darker than normal), perinuclear halo

Pap smear results requiring endometrial evaluation In women >/=45 endometrial cells (even benign) sign of endometrial hyperplasia or cancer

Colposcopy

If the cervical epithelium contains an abnormal load of cellular proteins

-> acetic acid coagulates the proteins -> opaque and white

Cervical biopsy:

Normally cervical epithelium matures and there are more flattened cells at the top

Abnormal: Lack of mature epithelium, no flattening of cells, big nucleus at the top

Cone biopsy if other dx indeterminate but high suspicion

Tx of CIN

LLETZ or LEEP: Dx+Tx AKA Conization

Complications: Shortens cervix, Stenosis of cervix, prolongs labour

Cryosurgery

Tx: Stage 1/2: Local extension: Total hysterectomy + LNs; Radiotherapy

Stage 3/4: Extensive radiotherapy and chemo/Palliative

Radiation: Vaginal stenosis, infection, fistula, dysparenia

Follow up post gyne cancer: 5 years

Every 3 months for 2 years, every 6 months for 2 years, then annually

If PAP suspicious yet entire squamocolumnar junction not visualised on colposcopy:

endometrial curettage (samples tissue from transformation zone)

Vulvar Cancer

Etiology: persistent HPV infection; chronic inflammation

RF: Smoking; Vulvar lichen Sclerosus; Immunodeficiency; Prior cervical cancer; Vulvar/CIN

Vulvar pruritus, vulvar plaque/ulcer, abnorm bleeding

Unifoical firm, white plaque often over labia majora —->> can become pruritic, friable and ulcerated

Dx: Biopsy

Vaginal Cancer

Vaginal bleeding

Malodorous discharge

Irregular lesion

RF: Age >60; HPV; Tobacco; In utero DES (Clear cell adenocarcinoma only)

Bartholin Duct Cyst

D/t blockage of gland duct

Vaginal pressure and discomfort w sexual activity

Behind posterior labium majus w poss extension into vagina

Tx: Observation and expectant management is asymp -> most spontaneously drain

Symptomatic/abscess —> incision and drain

Gartner duct cyst and Skene (paraurethral/lesser vestibular) gland cysts in Anterior vagina

Ovarian Tumours

Any large mass (>5cm) can induce torsion

Spread by seeding: transcoelemic (body fluid)———> spreads widely!!!

Dx: Pelvic US

Ca-125: can also go up in chronic smokers, endometriosis and infection

Laparoscopy

Benign Tumours: Differentiated

Functional cysts (d/t monthly follicle or corpus luteum)

Teratomas (dermoid/mature)

Solid fibromas

Endometriotic cysts (chocolate cyst)

Always evaluate adnexal mass: Pregnancy test and Pelvic US

Malignant masses appear complex (solid & cystic) with irreg, thickened internal septations

Epithelial cell tumours:

Papillomas: Surface epithelium -> ciliated

Unilocular/multilocular thin walled cyst -> clear serious fluid

Adenomas: Glandular epithelium (serous cystadenoma has FT like epi)

Unilocular, thin walled cyst -> Contain clear fluid

Brenners (some can be malignant):

Transitional epithelium with coffee bean nuclei; yellow/tan

Meigs Syndrome: Pleural effusion; ascites and BENIGN Ovarian tumour

Simple cyst occurs when follicle fails to rupture during ovulation

Functional Cyst

Follicular cysts: Lined by Granulosa cells

Corpus Luteal cyst/ Haematoma -> Bleeding within follicle

Increase progesterone level -> Delay in menstruation—> heavy periods

Unilateral pain

Sx: Bloating, change in urine/bowel habits eg incontinence

Positional Abdo pain (cyst moves with movement)

Rupture: bleeding if on anticoagulation

Torsion compresses blood vessels—-> Gangrene, shock

Tx: <5cm And asymp just observe

Surgery, can drain but tend to grow back! Aspirate cysts first as easier to remove

Ruptured cyst

Sudden onset severe, unilateral abdo pain immediately following strenuous/sexual activity

—>> becomes increasingly diffuse, often radiating to the shoulder (phrenic N irritation)

US: Pelvic free fluid

Peritoneal signs and hemodynamic instability

Theca Lutein and Granulosa Lutein cysts

Multiple and bilateral enlarged multi cystic ovary

RF: Multigestation; PCOS; Clomiphene (ovulation induction)

Circulating beta hcg causes hyperplasia of theca interna cells

Can cause hyperandrogenism

Associated with Hydatidiform mole/choriocarcinoma and hyper stimulation syndrome

Often regress once beta hCG levels normalise

Endometriotic cyst/ endometrioma/ Chocolate cyst

Most important clinical manifestation of endometriosis

Thick, white enlarged ovary; Unilocular adnexal mass

Dark brown discharge (blood/chocolate)

Constant pelvic pain

If on myometrium—-> excessive bleeding

Other locations——-> pain (worsens on exercise and intercourse)

Dermoid cyst (mature teratoma)—— seen in adolescents also

Tissue derived from 2 or more germ layers

Torsion: elevated risk d/t heterogeneity

Ovarian ischaemic and necrosis d/t obliteration of vessels -> decreased Doppler

Struma Ovarii derived from thyroid tissue

Unilocular with greasy yellow fluid Complex adnexal mass; echogenicity d/t hair; calcifications

Malignant Tumours:

Cyst adenocarcinoma —> epithelial tumours

Serous cystadenocarcinoma (psammoma bodies)

Germ cell tumours/ sex cord tumours

—->> Granulosa, Sertoli-Leydig Cell, Dysgerminoma, Immature teratoma, Yolk Sac

Secondary ie Krukenburg (stomach), uterus

Risk Factors: Unopposed Oestrogen

Ovulation inducing tx for infertility (care with clomiphene)

NMDA R antibodies

Management: US (if cyst/tumour)——> BLOOD TEST (CA125)

Blood test positive—-> laparotomy——> chemo

Blood test negative——> laparoscopy, cystectomy/oopherectomy

Tx: Total Abdo hysterectomy with bilateral salphingo opherectomy (ovaries useless at this point)

Store eggs for surrogacy

Granulosa Cell Tumour: Increased E2 and Inhibin

Juvenile subtype: Precoscious puberty

Call-Exnar Bodies (rosette pattern)

AUB

Bilateral breast tenderness and fibrocystic changes d/t increased breast tissue proliferation

Endometrial prolif d/t E2—-> thickened (>4mm) stripe —->>> Secondary endometrial cancer

Managment: Staging

Sertoli Leydig Cell Tumour: Elevated AFP and testosterone

Severely elevated testosterone —>> virilisation

Testosterone inhibits hypothalamic GnRH and pituitary FSH/LH release

——>> sx of oestrogen deficiency

—->> breast atrophy, vulvovaginal atrophy and dryness, dyspareunia and oligomennorhea

Young F

Px good

Dysgerminoma: Increased LDH and hCG -> hardcore gnomes

Fried egg cell appearance

Equivalent to seminoma in M

Immature teratoma: fetal tissue and neuroectoderm

Yolk Sac (endodermal sinus) Tumour

Schiller Duval Bodies (resemble glomerulus) and increase AFP

Embryonal Carcinoma

Aggressive w high beta hCG

Adolescents

Epithelial Ovarian Carcinoma

Acute: SOB, Obstipation/constipation with vomiting (bowel obstruction), abdo distension, DVT

Subacute: Pelvic/Abdo pain, bloating, early satiety

US: Solid mass with thick spectators; ascites

Metastatic spread —-> pleural effusion

Tx: Exploratory laparotomy with tumour debulking followed by platinum based chemo

Pseudomyxoma Peritonnei

Caused by cystadenomas of appendix and mucin producing tumours of ovary

—-> Appendix also most commonly associated

Mucin containing cysts with calcified rims

Calcifications can spread diffusely throughout peritoneum

Increased abdo girth, n+v

Tx: Surgical