Gynecology Flashcards
Discuss sex differentiation
- sex differentiation occurs through the SRY gene on the Y chromosome
- gene encodes for testis-determining factor -> mullerian inhibiting substance and testosterone which develop the male genital system
Discuss the development of the ovaries
- undifferentiated until the 7th week where develops from the paraxial mesoderm in 3rd week and develop the urogenital ridge around the nephrogenic cord in 4th week
- with no Y chromosome the indifferent gonad develop the ovary where the medullary cords degenerate, cortical cord develops (form future follicular cells) and no tunica albuginea
- ovaries descend slightly and the suspensory ligament develops from the superior genital ligament and the round ligament develops from the inferior genital ligament (gubernaculum)
Discuss the formation the genital Ducts
Indifferent Stage
- mesonephric duct is Wolfian duct
- paramesonephric duct is muellerian duct
Absence of MIS and Testosterone
- mesonephric duct degenerates
- paramesonephric duct develops to form the uterine tube, uterus and superior aspect of the vagina
- absence of testosterone forms the external genitalia and lower 1/3 of clitoris -> 5th month the vaginal plate canalizes to form the vagina
Discuss the formation of the external genitalia
Indifferent
- 3rd week mesynchymal cells migrate around cloacal membranes to form cloacal folds -> superiorly form genital tubercle and inferiorly form the urethral and anal folds
Development of External Genitalia
- genital tubercle elongates to form the clitoris
- urethral folds do not fuse to form labia majora
- urogenital groove remains open and form the vestibule
List the timing of events of the endometrial and ovarian cycles
Endometrial - day 1-5 have menstruation - day 6-13 have proliferative phase - day 15-28 have secretory phase Ovarian Cycle - day 1-13 have follicular phase - day 14 have ovulation - day 15-28 have luteal phase
Describe in-detail the ovarian cycle
Primordial
- primordial follicle develop into primary and then secondary follicle overtime and is gonadotropin independent -> larger primary oocyte with more zona pellucida + granulosa cells proliferating forming layers around oocyte + interstitial cells form theca cells around oocyte
Follicular Phase
- increase in FSH and LH lead secondary follicle to form the Graafian follicle, where fastest primary follicle to form secondary will be chosen
- tertiary follicle begin to produce estrogen which inhibits FSH causing other follicles to die
- dominant produce more estrogen leading to LH surge
Ovulation
- LH surge lead to ovulation by increasing antral fluid and release of hydrolytic enzymes so that secondary oocyte with corona radiata are release
- completion of meiosis 1
Corpus Luteam Phase
- corpus luteum produces progesterone and estrogen
- in the absence of LH the corpus luteum will degenerate into corpus albicans
- with bHCG the corpeus luteum will continue to release progesterone until taken over by placenta at 4-5 months
Describe the endometrial stages
Menstruation
- due to low estrogen and progesterone cause shedding of the endometrium
Proliferative
- high estrogen from follicle stimular endometrial cells increase its thickness
Secretory
- with high progesterone cause endometrial hypertrophy, thickening of the spiral arteries and glycogen secretion
Discuss where the major hormones of menstruation are produced
Progesterone
- produced by granulosa, theca, interstitial and corpus lutem
- LH stimulate corpus luteum to produce
- low <2 before ovulation and >5 after
- act on hypothalamus to decrease GnRH production
Testosterone
- produced by theca, interstitial and corpus luteum
- theca cells synthesize and then pass to granulosa cells via basement membrane to produce estrogen
- in non-dominant follicle cannot convert testosterone quickly enough resulting in atresia
Estrogen
- produced by granulosa and corpus luteum
- low <50 at menstruationa nd then peak at 200 during follicular development
- inhibit GnRH release
- FSH target granulosa cells to produces estrogen and stimulate follicular growth
Activin and Inhibin
- released by granulosa cells to activate or inhibit FSH release
Discuss the components, mechanism and use of oral contraceptive pill
Component
- low dose estrogen and progestin
Mechanism
- inhibit ovulation
- change cervical mucus
- cause pseudodecidualization of endometrium to inhibit implantatation
- inhibit tubal peristalsis to prevent fertilization
Use
- start at either 1st Sunday after menses, day 1 of month or immediately
- takes 7 days before it can work
- 21/7 method where hormone free days allow for menstruation
List the contraindications to OCP
- smoker and over age of 35
- <6 weeks post partum if breastfeeding
- history of VTE
- current breast cancer
- uncontrolled hypertension
- ischemic heart disease
- complicated valvular disease
- history of stroke
- migraine headache with aura or over 35 with migraine
- severe diabetes or cirrhosis
- SLE and APLA
- thrombophilia
List the benefits of OCP
Short Term
- regulation of menstrual cycle and decreased bleeding
- decreased dysmenorrhea, acne or premenstrual syndrome
Long Term
- decrease risk of endometrial, ovarian, and colorectal cancer
- decrease risk of benign breast disease
Other
- decrease risk of PID and ectopic pregnancy
- decrease risk of ovarian cyst
- improve endometriosis
Discuss the contraceptive patch and vaginal ring
- same as oral contraceptive where use for 3 weeks with 1 free week
Discuss the benefits of the progestin only pill
Mechanism - need to take pill everyday at same time and it increases cervical mucous - still have regular menstruation Indication - breastfeeding women or those with previous VTE Adverse Effects - irregular bleeding - worsening mood
Discuss the benefits of injectable progestin DMPA
Mechanism - inhibit ovulation - thicken cervical mucous - pseudodecidualization Use - injection every 3 months where have 2 week interval at mark where still effective Contraindication - known or suspected pregnancy - unexplained vaginal bleeding - current breast cancer Adverse Effect - 50% develop amenorrhea after 1 year and 75% after 2 years - weight gain due to increase appetite - decreased bone densit - delay to fertility: require 9 months after to return Benefit - treat menorrhagia, dysmenorrhea and endometriosis - treat menses related symptoms - decrease risk of endometrial and cervical cancer - decrease seizure
List the contraindications to an intra-uterine device
Contraindications - known pregnancy - puerperal sepsis - immediate post septic abortion - current PID or STI - cervical or endometrial cancer - current breast cancer - unexplained vaginal bleeding - distorted uterine cavity - malignant trophoblastic disease Adverse Effects - unscheduled vaginal bleeding - pain or dysmenorrhea - uterine perforation - infection - expulsion - failure where have increased risk of ectopic
Discuss the benefit of copper IUD
Mechanism
- foreign body reaction that lead to endometrial change that adversely affect sperm transport and inhibit sperm motility directly
- best used for emergency contraception 7 days post
Discuss the benefit of a mirena (LNG-IUS) IUD
- contain progesterone
- last up to 5 years
Mechanism - thicken cervical mucous
- suppress endometrial estrogen and progestin receptor
- inhibit ovulation
- inhibit implantation
- induce endometrial changes
Discuss the use of Plan B/Norvelo
- progesterone only Mechanism - inhibit ovulation - change endometrium to prevent implantation - disrupt luteal phase - effect on tubal transport - does not disrupt established pregnancy
Discuss the approach to primary amenorrhea
- failure to reach menarche (amenorrhea and no pubertal development by 14 or amenorrhea with secondary sexual characteristic by 16)
Pelvic Examination - if absent uterus must assess if have sexual hair -> if yes than mullerian agenesis and if no then CAIS
- if normal then assess bHCG
Negative bHCG assess prolactin, TSH and FSH
Prolactin - if increased require MRI head to assess for pituitary tumour
- treat with surgery or dopamine agonist
TSH - if elevated treat with thyroid replacement
FSH Decreased - assess if have eating disorder, over exercise or stress
- if no, then MRI for tumour -> if MRI negative than Kallman
FSH Increased - gonadal failure so must do karyotype assessing for primary ovarain insufficiency or Turner or fragile X
FSH Normal - testosterone increased than ovarian sonography for tumour
- DHEAS high then adrenal MRI for tumour
- if DHEAS and testosterone normal or high normal than PCOS
- 17-OH-P increased than congenital adrenal hyperplasia
List the differential for secondary amenorrhea
Hypothalmic - eating disorder or stress Pituitary - prolactinoma Thyroid - hypothyroidism Ovary - PCOS - primary ovarian insufficiency
Discuss the presentation and management of primary ovarian insufficiency
- 90% are idiopathic and then Turner or chemo/radiation
Pathophysiology - inadequate follicles to sustain menses due to failure tof form enough primordial follicles or accelerated loss or damage
Presentation - primary or secondary amenorrhea
- menses interal >90 days
- oligomenorrhea
Investigation - consistently high FSH and LH
- consistently low estradiol
Diagnosis - primary or secondary amenorrhea for 3 months or changes from normal for 3 months
- high FSH >40 on 2 occassions a month apart
- age <40
Complications - increased risk of osteoporosis and atheroscleorsis
- infertility
Management - pre-puberty: increase estrogen over 2 years until breakthrough bleed -> add progesterone
- Post-Puberty: estrogen for 1-26 and progesterone for 14-26 of cycle (OCP or patch)
- prevent complications through lifestyle, monitoring and supplementation
Discuss the presentation and management of polycystic ovarian syndrome
Rotterdam Diagnosis (2/3) - oligo or anovulation - clinical or biochemical hyperandrogenism - polycystic ovaries (>12 follicles) Acute Management - menstrual irregularities with oral contraceptive - acne with lifestyle changes - hirsutism with spironolactone - infertility Surveillance - impaired glucose tolerance (possible pathophysiology where theca cell insulin resistance lead to unopposed estrogen with elevated LH) - endometrial hyperplasia - hyperlipidemia
Discuss the signs of hyperandrogensism
- hirsutism on androgen dependent areas of body
- acne
- clitoromegaly
- male balding
- obesity
- insulin resistance
List the differential for abnormal uterine bleeding
Structural Abnormalities (PALM) - polyp - adenomyosis - leiomyoma - malignancy No Structural Abnormality (COEIN) - coagulopathy - ovulatory dysfunction - endometrial - iatrogenic - not yet classified
Discuss the risk factors for polyp and risk factors for polyp malignancy
Risk Factors - tamoxifen - obesity - hormone replacement - age For Malignancy - >1.5cm - tamoxifen - age >60
Discuss the diagnosis and treatment of polyps
Diagnosis - hysteroscopy - saline infusion sonography Treatment - symptomatic or post-menopausal - asymptomatic if risk for malignancy, mulitple, prolapse, infertility
Discuss the presentation and management of adenomyosis
- are ectopic endometrial glands and stroma within myometrium resulting in enlarged uterus Presentation - heavy menstrual bleeding - painful menstruation with chronic pelvic pain - enlarged uterus Treatment - hysterectomy - hormonal therapy - ablation - embolization
Discuss the presentation and management of fibroids
- is growth of myometrial smooth muscle in women of reproductive age
Presentation - heavy and prolonged menses
- pelvic pain or pressure with 4 D’s (dysmenorrhea, dyspareunia, dyschezia, dysuria)
- infertility
- enlarged urterus
Investigations - CBC for anemia
- transvaginal ultrasound
Treatment - prophylactic if causing infertility, IVF or hydronephrosis
- hormonal therapy with OCP or menopause inducing drugs
List the risk factors for fibroids
Increased - African American - early menarche - family history - hypertension - obesity - alcohol - red meat Decreased - high parity - exercise - smoking - healthy diet
Discuss the screening and treatment of coagulopathy leading to AUB
Screen
- heavy menstrual bleed
- one of post-partum hemorrhage, surgery related bleed, bleeding with dental work
- two of bruising, epistaxis >=1/month, frequent gum bleeding, or family history
Treatment
- No pregnancy then contraceptive method
- pregnancy then antifibrinolytic, factor replacement, dDAVP