O&G Flashcards
Helpful videos
PRENATAL TESTING https://www.youtube.com/watch?v=_esAs0vVFd4
https://www.youtube.com/watch?v=_esAs0vVFd4&t=38s
PROM https://www.youtube.com/watch?v=MY7w76rC2rE
ECTOPIC https://www.youtube.com/watch?v=Q_qiUYIBR7o
PLACENTA PREVIA
https://www.youtube.com/watch?v=xnRIF8SDYf8
FETAL GROWTH ABNORMALITIES https://www.youtube.com/watch?v=t0k7LSx9iL0
PPH https://www.youtube.com/watch?v=FVvcmY9Skzc
NORMAL LABOR https://www.youtube.com/watch?v=cTTJoNQSXmo
OVARIAN PATHOLOGY
https://www.youtube.com/watch?v=oZeagsS6Fws
ENDOMETRIAL CANCER
https://www.youtube.com/watch?v=CJZr9_LATgQ
CERVICAL CANCER
https://www.youtube.com/watch?v=5KEAnfLj1pE
STAGE OF LABOR
https://www.youtube.com/watch?v=h7nOZ2kNfW4
PRE-ECAMPLSIA
https://www.youtube.com/watch?v=RB5s85xDshA
MENSTRUAL CYCLE
https://www.youtube.com/watch?v=tOluxtc3Cpw
GERM CELL OVARIAN TUMOURS
https://www.youtube.com/watch?v=8Ymvt2vBM1I
PID
https://www.youtube.com/watch?v=eYk3GdBw-28
Uterus changes during life
NEONATE
Cervix larger than fundus
PREPUBERTY
Tube like uterus with cervix and uterus same size
PUBERTY Pear like (adult) with fundus larger than cervix
Ovaries begin at 1cc until around 6yo then gradually increase in size
TURNER SYNDROME
XO kids. Horseshoe kidney, aortic coarctations, prepuberty uterus and streaky ovaries
Embryology
MULLERIAN DUCTS
Uterus, fallopian tubes, upper 2/3 vagina
WOLFFIAN DUCTS (SHOULD REGRESS) Vas deferens, seminal vesicles, epididymis
UROGENITAL SINUS
Prostate, lower 1/3 vagina
“stuff that makes kidneys and uterus is in same soup. pour soup down back of belly on both sides. upper part makes kidney, lower makes uterus. 2 puddles fuse in pelvis. clean up operation in pelvis to cleave to get central cavity capable of carrying baby”
Problems in embryology
FAILURE TO FORM
Only have soup on one side. No kidney on that side and usually have unicornuate uterus.
FAILURE TO FUSE
Soup fails to fuse in pelvis. On spectrum of no fusion with uterine didelphys to mostly fused bicornuate
FAILURE TO CLEAVE
Septate uterus
Failure to form
MULLERIAN AGENESIS
Mayer-Rikitansky-Kuster-Hauser syndrome
Vaginal atresia, absent or rudimentary uterus and normal ovaries. Kidneys have issues in half cases (agenesis/ectopia)
UNICORNUATE UTERUS - 4 VARIANTS
- unicornuate + communicating cavitatory rudimentary horn
- unicornuate + non-communicating cavitatory rudimentary horn
- unicornuate + non-cavitatory rudimentary horn
- isolated unicornuate (most common 35%)
If see unicornuate need to look for rudimentary horn. Horns can have endometrium which gives rise to many causes of pain . Increase risk of miscarriage and life threatening bleed if in noncommunicating horn as it can rupture
FAILURE TO FUSE
UTERINE DIDELPHYS
Complete uterine duplication (2 cervices, 2 uteri and 2 upper 1/3 vagina). Vaginal septum present 75% time.
BICORNUATE
Either one cervix unicollis or 2 bicollis. Seperation of uterus by deep myometrial cleft. Vaginal septum 25% time. Fetal loss much less of an issue than septate
T SHAPED
DES related anomaly. Historical trivia. DES synthetic oestrogen given to prevent miscarriage in 40s. Daughters of these patients had vaginal clear cell carcinoma and T shaped uterus
Failure to cleave
SEPTATE
Two endometrial canals separated by fibrous or muscular septum. Determine on MRI, this changes surgical management. Increased risk infertility and recurrent abortion. Septum has poor blood supply. Improved outcomes with resection of septum.
ARCUATE
mild smooth concavity of uterine fundus. Normal variant. Not associated with infertility or obstetric complications
Bicornuate vs septate
BICORNUATE
Heart shaped fundal contour. No significant infertility issues. Resection of septum has poor outcomes
SEPTATE
Fundal contour is normal. Infertility issues, implantation fails if on septum. Resection of septum can help.
HSG
Part of infertility workup or to prove success of tubal ligation.
Day 7-12 as least chance of pregnancy, also dont want to push endometrium through the tubes into pelvis.
Contraindications: pregnancy, active pelvic infection, active bleeding, contrast allergy
Irregular uterine filling defects may be scarring or adhesions (can be trauma from prior curettage). Round filling defects polyps or fibroids. Bubbles from not primed catheter.
Proximal blockage shows abrupt cutoff with no distal opacification. Distal blockage shows dilated tubes with no pelvic spillage.
Salpingitis Isthmica Nodosa (SIN)
Nodular scarring of fallopian tubes. Aunt Minnie.
Proximal 2/3 tube. Likely inflam/infect. Associated with infertility and ectopic preg.
Uterine AVM
Congenital or acquired (more common). Can have fatal bleed. Previous D+C can cause this, therapeutic abortion, caesarian section or multiple preg.
Serpiginous tubular anechoic structures within myometrium with high velocity flow
Intrauterine adhesions (Ashermans)
Scarring in uterus usually secondary to D+C, surgery or pregnancy. Can be infection/PID.
Either on HSG with irregular filling defects or MRI with T2 dark bands. Usually infertility results.
Endometritis
Spectrum of PID. 2-5 days after delivery, especially in prolonged labor or premature rupture. Fluid and thickened endometrial cavity. Can have gas in cavity.
Pelvic floor
3 compartments which are maintained by endopelvic fascia, levator ani and urogenital diaphragm.
ANTERIOR
Bladder and urethra
Cystocoele is bladder >1cm below pubococcygeal line
MIDDLE
vagina, cervix, uterus and adnexa
Uterine prolapse is descent of cervix or posterior vaginal fornix >1cm below pubococcygeal line
POSTERIOR
anus and rectum
Rectocoele is abnormal rectal bulging usually anteriorly, bulging relative to anal canal, due to weakness in rectovaginal fascia.
Fibroids (uterine leiomyoma)
Benign smooth muscle tumour - most common uterine mass. Like estrogen and most common in reproductive age. Grow rapidly in pregnancy and involute in menopause.
Can look like anything. Usually hypoechoic with peripheral blood flow and shadowing. Can have peripheral popcorn calcs
HYALINE (CLASSIC)
Most common. T1 dark T2 dark, homogenous enhancement
HYPERCELLULAR
Dense smooth muscle, respond well to embolization T1 dark, T2 bright, homogenous enhanement
LIPOLEIOMYOMA
Rare fat containing subtype. Hyperechoic on USS. Fatty uterine mass CT. Fat sat on MRI. T1 bright, T2 bright, rim enhancement
Degeneration
Lack enhancement. Can degenerate in 4 ways.
Classic - outgrows blood supply, get proteinaceous material
Red - in pregnancy due to venous thrombosis
Myxoid - uncommon
Cystic - uncommon
Uterine leiomyosarcoma
Risk of malignant transformation to this is low 0.1%. Look like fibroid but rapidly enlarge. Areas of necrosis often seen
Adenomyosis
Endometrial tissue that has migrated into myometrium. Most common in multiparous women of reproductive age, especially if history of uterine procedures.
Usually generalized but spares cervix. Can cause marked enlargement of uterus, especially posterior wall.
Can be shown on USS or MRI. Hyperechoic adenomyosis with hypoechoic muscular hypertrophy. MRI shows thickening of junctional zone to over 12mm (normal <5mm) which can be focal or diffuse. Small T2 bright cystic areas (Venetian blind artefact on USS)
Thick endometrium
Measured without fluid in canal. >5mm in postmenopausal women should be sampled. Premenopausal can get up to 20mm
Estrogen secreting tumours will thicken endometrium - granulosa cell tumours of ovary
HNPCC have 30-50 x risk of endometrial cancer
Post meno bleeding
Endometrium <5mm probably atrophy. Endometrium 4-5mm maybe cancer and gets biopsy
Tamoxifen changes
This is a SERM (selective estrogen receptor modulator). Acts like estrogen in pelvis, blocks estrogen effects in breast. Used for breast cancer but marginally increases risk of endometrial cancer 1% per year.
Can cause subendometrial cysts and development of endometrial polyps 30%. Tamoxifen endometrium often thick, up to 12mm
Endometrial fluid
In premeno this is common. In post meno may mean cervical stenosis or obstructing mass.
Endometrial cancer
90% adenocarcinoma. Possible exception leiomyosarcoma.
Usually post menopausal bleeding.
Step 1 USS for endometrial thickness. If thick biopsy if abnormal then MRI for staging
MRI
T1 iso, T2 mildly hyper, homogenous enhancement, restricted diffusion.
Staging via FIGO system
STAGE 2
disease defined as cervical stroma invasion, high risk for LN mets. Key is C+ phase, if normal cervical enhancement then no invasion. Changes management to preop radiation to cervix along with Radical hysterectomy rather than TAH.
STAGE 1A (<50% myometrium) to STAGE 1B (>50% myometrium) increases risk of LN disease.
STAGE 3
Local or regional spread
STAGE 4
Involvement of bladder or rectum
Cervical cancer
Usually squamous cell related to HPV (90%). Once you have parametrial invasion (stage2b) or involvement of lower 1/3 vagina it gets chemo/radio. Also FIGO staging.
STAGE 2A
Spread beyond cervix but no parametrial invasion - surgery
STAGE 2B
Parametrial involvement but no extension to sidewall - chemo/radio
PARAMETRIUM
fibrous band that separates supravaginal cervix from bladder. Extends between layers of broad ligament. Important as uterine artery is in here so need for chemo once invaded. Cervix normally has T2 dark ring, if this is lost its invaded beyond here.
Solid vaginal masses
Can be primary (clear cell adenocarcinoma or rhabdomyosarcoma) or secondary (cervical or uterine carcinoma protruding into vagina).
LEIOMYOMA
Rare in vagina but can occur usually in anterior wall
SQUAMOUS CELL CARCINOMA
Most common cancer of vagina 85%. Associated with HPV
CLEAR CELL ADENOCARCINOMA
Along with T shaped uterus in DES - historical and rare
VAGINAL RHABDOMYOSARCOMA
Most common tumour of vagina in kids. Bimodal age distribution 2-6 and 14-18. Anterior wall near cervix.Solid T2 bright enhancing mass in vagina/lower uterus in kid
Met to anterior upper vagina 90% upper genital tract
Met to posterior lower vagina 90% GIT
Cystic vaginal/cervical masses
NABOTHIAN CYSTS
Common, usually on cervix. Inflammation causing epithelium plugging of mucous glands
GARTNER DUCTS CYSTS
Result of incomplete regression of Wolffian ducts. Along anterolateral wall of upper vagina. If at urethra can cause mass effect on urethra.
BARTHOLIN CYSTS
Obstruction of Bartholin glands (mucin secreting glands from urogenital sinus). Below pubic symphysis. If infected can suture open to allow continual drainage. “Bartholin Below
SKENE GLAND CYSTS
Cysts in these periurethral glands can cause recurrent TI and urethral obstruction
Ovary
Ovarian volume normal up to 15ml. Post meno shouldnt be over 6ml.
Follicles seen in early cycle are <5mm. By day 10 a dominant follicle emerges up to 20mm. Follicle then ruptures, releases egg and forms corpus luteum. Can have physiologic fluid in pelvis at this time
CUMULUS OOPHORUS
Collection of cells in mature dominant follicle that protrude into follicular cavity and signal imminent ovulation
Theca lutein cysts
Type of functional cyst related to overstimulation from bHCG. Large cyst with multilocular cystic appearance - spoke-wheel
Multifetal pregnancy
Gestational trophoblastic disease (moles)
Ovarian hyperstimulation syndrome
Ovarian hyperstimulation syndrome
Complication associated with fertility therapy (5%). Ovaries with theca lutein cysts, then ascites and pleural effusions. May also have pericardial effusion. Risk of ovarian torsion and hypovolaemic shock
Paraovarian cyst
Cyst in adnexa but not in ovary. Adjacent to ovary or tube. Very low rate of malignancy.
Post meno ovary
Abnormal if it either exceeds upper limit of normal or is twice size of other ovary. Small cysts seen in around 20% post meno. Post meno ovaries are atrophic, lack follicles and can be difficult to find.
Ovarian volume will decrease from 8cc at 40 to 1cc at 70. Max ovarian volume post meno is 6cc.
Not simple cyst if irregular septations, papillary projections or solid elements
Benign ovarian masses
Physiologic and functioning follicles Corpus Luteum Haemorrhagic cysts Endometrioma Benign cystic teratomas (dermoids) Polycystic ovaries
Functioning ovarian cysts/follicles
Affected by menstrual cycle. Benign and usually <25mm. Will change/disappear in 6 weeks. If it doesnt change/disappear it is considered nonfunctioning (not under hormonal control)
Simple cysts >7cm may need MRI evaluation. Risk torsion.
Corpus Luteum
Normal CL arises from dominant follicle. Can be large 5-6cm with variable appearance. Most common is solid and hypoechoic with ‘ring of fire’. Thin echogenic rim. Moves with ovary
CL vs ectopic:
Both can have ‘ring of fire”. Most ectopics in tube, CL is in ovary. Ectopic usually hyperechoic to ovary, CL hypoechoic to ovary. Ecopic has thick echogenic rim and moves separate to ovary
Endometrioma
Targets young women in reproductive years. Can cause chronic pelvic pain with menstruation.
Triad of infertility, dysmenorrhoea and dyspareunia
Rounded mass with homogenous low level internal echoes and increased through transmission 95% cases
Dont tend to change on follow up (haemorrhagic cysts do). Can have small echogenic foci adhering to walls.
Most common location for endometriosis is uterosacral ligts and in or near c section scar.
1% endometriomas become malignant to endometroid or clear cell carcinoma. Malignancy very rare in endometrioma <6cm, usually larger than 9cm. lso usually >45yo
Endometrioma T1 bright from blood, T2 dark from iron (shading sign)
Haemorrhagic cyst
A ruptured follicle can bleed internally and re-expand. Homogenous mass with increased through transmission. Similar look to endometrioma, lacy fishnet appearance. Doppler absent.
Haemorrhagic cyst will go away in 1-2 cycles, endometrioma wont.
Post meno will occasionally ovulate. Follow in 6-12 weeks.
Dermoid
Usually in young women 20-30 and are most common ovarian neoplasm in patients <20. “tip of iceberg” sign is classic buzzword and refers to absorption of most of USS beam at top of mass.
Cystic mass with hyperechoic solid mural nodule (Rokitansky nodule or dermoid plug). Septations in 10%
MRI T1 bright from fat and will suppress on FS imaging (endometriomas and haemorrhagic cysts wont).
1% malignant transformation usually to squamous cell ca. Risk factors size >10cm and age >50.
Endometrioma - clear cell
Dermoid - squamous
PCOS
Typically overweight girl with acne, pencil moustache.
> 10 peripheral simple cysts <5mm. String of pearls appearance
Ovaries enlarged >10cc although 30% will have normal volume
Ovarian masses - think malignant if
Complex cystic adnexal masses with thick septations and papillary projections (nodule with blood flow)
Solid adnexal masses with variable necrosis
Serous ovarian/Cystadenocarcinoma/Cystadenoma
Serous are most common type of ovarian malignancy.
60% serous tumours benign and 15% borderline, remaining are malignant.
Women of childbearing age. Typically unilocular with few septation. Papillary projections common and suggest malignancy.
If ascites, 70% have mets (70% have peritoneal involvement at time of diagnosis)
Mucinous ovarian cystadenocarcinoma
Often large mass. Typically multiloculated although septa are thin. Papillary projections less common. Can get low level echoes from mucin.
Get pseudomyxoma perotineii with scalloping of solid organs.
Serous vs mucinous
SEROUS
Unilocular with few septations
Papillary projections common
MUCINOUS
Multilocular with more septations
Papillary projections less common
Endometroid ovarian cancer
Second most common ovarian cancer (serous 1, mucinous 3)
Bilateral 15% time. 25% women will have concomitant endometrial cancer (ovary is met).Endometriomas can turn into this rarely.
Ovarian mass + endometrial thickening will be endometrioid cancer OR granulosa theca cell tumour which produce estrogen and cause endometrial hyperplasia
Large mass differential
BFM in adult:
Ovarian masses mucinous and serous
Desmoids
Sarcomas
BFM in kid:
Askin tumour (PNET/Ewings)
Pleuropulmonary blastoma
Fibroma/Fibrothecoma
Benign ovarian tumour in middle aged women. Similar to fibroid.
USS hypoechoic and solid. MRI T1 and T2 dark with band of dark T2 signal around tumour on all planes. Calcs rare
Similar conditions
Meigs syndrome = ascites, pleural effusion and benign ovarian tumour
Brenner tumour = epithelial tumour of ovary in women 50-70s. Fibrous and T2 dark. Calcs common 80%
Struma ovarii
Subtype of ovarian teratoma. Multilocular cystic mass with intensely enhancing solid component.
MRI low T2 signal in cystic areas which is colloid. Tumours contain thyroid tissue. Clue may be patient hyperthyroid or in thyroid storm.
Ovarian mets
10% of malignant ovarian tumours are mets. Primary most commonly colon/gastric/breast/lung and other ovary. Bilateral solid tumours classic
KRUKENBURG TUMOUR
Mets to ovary from GIT usually stomach
Ovarian torsion
Rotation of ovarian vascular pedicle resulting in arterial or venous obstruction. Typically associated with cyst or tumour. Has dual blood supply so flow less accurate in diagnosing.
Most constant finding is large ovary. Unilateral large ovary over 4cm Mass on ovary Peripheralised cysts/follicles Free fluid Lack of arterial or venous flow.
Hydrosalpinx
Buzzword is “cogwheel appearance” referring to normal longitudinal folds of fallopian tube becoming thickened/ “string sign: is incomplete septae. “waist sign’ is tubular mass with indentations of its opposing walls.
Most common cause PID. Can also be endometriosis, tubal cancer, post hysterectomy and tubal ligation.
Pelvic Inflammatory Disease
Infection or inflammation of upper genital tract. Will see hydrosalpinx with ill defined margin of uterus. Can progress to tubo-ovarian absess and can get bowel or urinary changes.
Paraovarian cyst
Congenital remnant from Wolffian duct. Do not distort adjacent ovary. Can mimic exophytic cyst but are separate to ovary
Ovarian vein thrombophlebitis
Usually in postpartum women with acute pelvic pain and fever approx 10 days after delivery. 80% time on right. Tubular structure with enhancing wall and thombus
Peritoneal inclusion cyst
Inflammatory cyst of peritoneal cavity that occurs when adhesions envelop an ovary. Adhesions cannot absorb fluid. Expanding pelvic mass from normal secretions by active ovary..
Classic is patient with prior pelvic surgery now with pain. Could say with history of PID or endometriosis, needs to occupy pelvic recess and contain the ovary.
Lacks walls, passive shape that conforms to surrounding structures. Entraps ovary
Gestational trophoblastic disease
Marked bHCG rise. Hyperemesis often part of stem. Moles common in age >40 and prior moles make you more likely to get another.
Hydatidiform mole
Most common form, benign. 2 subtypes
COMPLETE MOLE
Classic, 70%. Involves entire placenta with no fetus. Pathogenesis is fertilization of an egg which has lost its chromosomes.
1st trimester USS shows uterus filled with echogenic solid highly vascular mass described as “snowstorm”
2nd trimester USS vesicles that make up mole enlage into individual cysts. “Bunch of grapes”
PARTIAL MOLE
30%. Only portion of placenta. Fetus present but triploid. Fertilization of an ovum by 2 sperm. Lethal to fetus
US placenta enlarged with areas of multiple diffuse anechoic lesions and may see fetal parts.
Can see theca lutein cysts in molar pregnancies
Invasive mole
Invasion of molar tissue onto myometrium. Can see it after treatment of hydatidiform mole. Echogenic tissue in myometrium. MRI better to see muscle invasion. Focal myometrial masses, dilated vessels and areas of haemorrhage/necrosis
Choriocarcinoma
Very aggressive malignancy that forms only trophoblasts. Spreads locally into myometrium and parametrium then haematogenous to any site of body. Very vascular. Classic scenario is bHCG rising following evacuation of molar pregnancy. USS shows highly echogenic solid mass. Treatment is methotrexate.
Penile fracture
Fracture of corpus cavernosum and surrounding sheath, the tunica albuginea.
T1 axial. Black line tunica albuginea will be interrupted. Look for haemorrhage in corpus cavernosum.. Stigmata can be suboptimal angulation (Peyronie’s) from fibrous scar formation
Prostate adenocarcinoma pattern
Peripheral zone 70%. Most common cancer obv
Transition zone 20%
Central zone 10%.
Central gland Most common BPH
Cancer is T2 dark with restricted diffusion, early enhancement and rapid washout
If PSA <20 very low chance of bone mets. Bone scan is best study for prostate mets
Prostate staging
STAGE 2
Confined by capsule T2
Abutment of capsule without bulging
STAGE 3
Extension through capsule (T3a)
Bulging of capsule or extension through it
Extension through capsule is most important factor governing treatment.
Seminal vesicles and nerve bundle are behind prostate and can get invaded.
Prostate Ca
1/6 men will get it and 3% die from it. People who die are:
Gleason scores 8-10
Advanced clinical stage (mets)
PSA>20
People with Gleason <6, PSA <10 and staging <2a are unlikely to die of prostate ca
Most say hormone therapy around stage 2b
PSA
Antigen produced by normal prostate and incorporated into ejaculate for the purpose of dissolving cervical mucus. Also leaks out into blood in small amounts normally or larger when prostate damaged.
Post prostatectomy, normal is 0. Should think recurrence when >0.2. After radiation anything >2 is abnormal
Gleason
Grade, score and group.
GRADE
Histological pattern
1 normal, 5 very abnormal, rest inbetween
SCORE
Sum of two most common grades. More common pattern always first. Scores less than 6 not usually reported.
GROUP
Uses pattern scores to reflect actual risk. Removes confusion over one 7 being worse than another.
PIRADS
Scores calculated using data from DWI, T2 and enhancement. Tumour in transition zone is determined primarily from T2 (all T’s), peripheral zone is from DWI
Benign prostatic hypertrophy
Very common. Volume of 30cc used as cutoff. Most commonly involves transitional zone (central gland) where cancer is rare. Median lobe is the one that hypertrophies and protrudes up into bladder.. Can cause bladder outlet obstruction, wall thickening and diverticulae
Buzzword is J shaped or fish-hook or Hockey stick ureter as this curves around enlarged prostate into bladder
BPH NODULES Transitional zone (central gland) T2 heterogenous Can restrict diffusion May enhance and washout