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3rd year - Obstetrics and Gynecology > Gynecology (Tony's) > Flashcards

Gynecology (Tony's) Flashcards

1
Q

Sex determination

A

Chromosomal sex determined at conception (XX, XY)

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2
Q

Sex differentiation

A

Development of male or female urogenital system which involves sex and autosome chromosome genes

Genotypic/primary sex differentiation - development of gonads

Phenotypic/seconday sex differentiation is development of the urogenital system

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3
Q

Male sex differentiation

A

Y chromosome contains SRY (sex determining region) gene, which encodes TDF (testis-determining factor)

TDF initiates cascade of downstream events to develop male urogenital system (mullerian inhibiting substance (MIS) + testosterone to develop male urogenital system)

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4
Q

Female sex differentiation

A

Default pathway is female (absence of SRY gene)

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5
Q

Development of the ovaries

A
  1. Gonadal ridges in the mesoderm
  2. Primordial germ cells develop in endoderm of yolk sac and migrate via dorsal mesentary to invade the genital ridges
  3. Celoemic epithelium gives rise to primitive sex chords, which penetrate the underlying mesenchyme
  4. In male develop into testis (primitive sex chords develop to form seminiferous tubules and tunica albuginea thickens)
  5. In female develop into ovaries (primitive sex chords develop to form medulla of ovary and tunica albuginea disappears) and surface epithlium gives rise to secondary sex cords (become follicular cells)
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6
Q

Descent of ovaries location and support

A

Ovaries move inferiorly and settle just below the rim of the true pelvis.

The superior (cranial) genital ligament forms the suspensory ligament of ovary.

The inferior (caudal) genital ligament (aka gubernaculum) forms the ovarian ligament and round ligament of uterus

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7
Q

Genital duct development

A
  1. Indifferent stage - mesonephron (Wolfian) duct develops if male and paramesonephric (Muellerian) duct develops if female
  2. Sex differentiation of genital duct
    MIS and testosterone presence or absence
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8
Q

Role of testosterone in the differentiation of the genital duct

A

Testosterone stimulates development of mesonephric duct and stimulates development of male external genitalia
Absence results in disintegration of mesonephric duct and development of female external genitalia (labia majora, labia, minora, clitoris and lower 2/3 vagina)

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9
Q

Role of MIS in sex differentiation of genital duct

A

MIS - inhibits development and stimulates disintegration of paramesonephric duct which develops into uterine tube, uterus and superior part of vagina

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10
Q

Formation of uterus

A

Bilateral paramesonephric ducts fuse at the distal end to become uterus and superior part of vagina and septae eventually disappears

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11
Q

Formation of vagina

A

Dual origin where the superior part is derived from paramesonephric duct and the inferior part is derived from urogenital sinus

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12
Q

What are the components that make up the pelvic brim

A
  1. Sacral promontory
  2. Margin of sacral ala
  3. Arcuate line of ilium
  4. Pectineal line
  5. Pubic crest
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13
Q

What is the pelvic outlet

A

plane bounded by tip of coccyx posteriorly; sacrotuberous ligament posteriolaterally; ischial tuberosities laterally; ischiopubic rami and pubic symphysis anteriorly

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14
Q

What is the pelvic diaphragm and its components

A

Funnel shaped muscular floor composed of floor of lesser (true) pelvis and roof of perineum

Made by coccyges and levator ani (pubococcygeus, iliococcygeus) muscles

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15
Q

What is the pelvic brim

A

Divides the superior greater (false) pelvis and inferior lesser (true) pelvis

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16
Q

What are the conjugate measurements of the pelvis

A

Anatomical (true) conjugate
Obstetric conjugate
Diagonal conjugate

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17
Q

True conjugate

A

Distance from sacral promontory to superior aspect of pubic symphysis

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18
Q

Obstetric conjugate

A

distance from sacral promontory to most posterior aspect of pubic symphysis

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19
Q

Diagonal conjugate

A

distance from sacral promontory to inferior aspect of pubic symphysis

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20
Q

What is the transverse diameter of pelvic outlet

A

distance between ischial tuberosities (10-11cm)

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21
Q

What is interspinous diameter

A

distance between ischial spines

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22
Q

What penetrates the pelvic diaphragm

A

Urethra, vagina, rectum

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23
Q

What is the role of the medial fibers of levator ani (part of pubococcygeus)

A

Forms sling around rectum (puborectalis)

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24
Q

What is the role of the pelvic diaphragm

A

supports pelvic viscera, contribute to fecal / urinary continence

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25
Q

What is a lateral episiotomy

A

Controlled incision of pelvic diaphragm

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26
Q

Pelvic diaphragm compromise and consequences

A

due to damage during childbirth in female or prostatectomy in males, increasing risk of organ prolapse

in female, primary uterus and bladder prolapse

organ prolapse lead to urinary and fecal incontinence in both genders

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27
Q

Where does the coccygeus muscle run

A

Inside aspect of sacrospinous ligament

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28
Q

What is the levator plate

A

pubococcygeus and iliococcygeal muscle form shelf like portion of pelvic floor behind the anus

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29
Q

What is the Pouch of Douglas and its significance

A

Rectouterine pouch where pus and fluid collects, which can be drained through posterior fornix

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30
Q

Components of broad ligament

A

Mesoosalpinx
Mesometrium
Mesovarium

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31
Q

What forms the broad ligament of the uterus

A

Peritoneum drapes over the uterus, uterine tube and ovary superiorly

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32
Q

What is the parametrium

A

Covering that separates the uterus from the bladder

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33
Q

Pubocervical ligament role

A

Fascial ligament that anchors side of cervix to pubic symphysis

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34
Q

What are the uterine fascial ligaments

A

Deep - underneath the broad ligament (peritoneum) that support the position of the uterus

Part of the parametrium

Pubocervical ligament, transverse cervical ligament, uterosacral ligament

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35
Q

Pubocervical ligament

A

Anchor side of cervix to pubic symphysis

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36
Q

Transverse cervical ligament

A

aka Mackenrodt or transverse cardinal ligament

Provides central cervical support and carries the uterine artery

Ureter inferior to the transverse cervical ligament/uterine artery

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37
Q

Uterosacral ligament

A

Anchor cervix posteriorly to sacrum

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38
Q

Ovarian ligament role

A

Tethers ovary to uterus

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39
Q

Round ligament role

A

Tethers uterus through inguinal canal to labia majora

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40
Q

What is the isthmus

A

Initial narrowing from body of uterus to cervix

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41
Q

Layers of uterus

A

4 layers from superficial to deep

1) Parametrium - supporting fibrous fascia (transverse cardinal/cervical ligament, uterosacral ligament, pubovesical ligament)
2) Perimetrium - peritoneal coat overlying uterus, continuous with mesometrium of broad ligament
3) Myometrium - smooth muscle
4) Endometrium - internal mucosa

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42
Q

What is the angle of version of the uterus

A

Angle between vaginal and cervical axis

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43
Q

What is the angle of flexion of the uterus

A

Angle between uterine body axis and cervical axis

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44
Q

What is the most common orientation of the uterus

A

Anteverted and anteflexed

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45
Q

Components of the uterine tubes

A

Infundibulum –> ampulla –> isthmus –> intrauterine part –> horns of uterus

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46
Q

Where are the ovaries located

A

Ovarian fossa, medial to external iliac vessel and anterior to ureter and internal iliac artery

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47
Q

What are located at the vaginal uterine junction

A

4 vaginal fornices - 1 anterior, 1 posterior, 2 lateral

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48
Q

What is the suspensory ligament of ovary

A

Mesentery overlying ovarian artery and ovarian vein

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49
Q

Ovarian blood supply and drainage

A

Ovarian artery from abdominal aorta

Ovarian vein drains into IVC

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50
Q

Uterine blood supply and drainage

A

Uterine artery from internal iliac artery

Uterine vein drains into internal iliac vein

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51
Q

Vaginal blood supply and drainage

A

Vaginal artery from internal iliac artery and internal pudendal artery from internal iliac artery (feeds distal vaginal canal in perineum)
Vaginal and internal pudendal veins drain into internal iliac vein

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52
Q

Pelvic blood supply

A

Internal iliac artery with anterior and posterior division

Anterior - supplies pelvic viscera
Anterior division includes umbilical artery, superior vesicle artery, uterine artery, vaginal or inferior vesicle artery and middle rectal artery and internal pudendal artery

Posterior division goes to body wall, lower limb muscles, perineum

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53
Q

Uterine artery

A

Pass above ureter
Tortuous
Runs in transverse cardinal ligament

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54
Q

Superior vesicle artery

A

Feeds superior aspect of bladder and comes off umbilical artery

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55
Q

Vaginal/inferior vesicle artery

A

Feeds inferior aspect of bladder and superior vagina

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56
Q

Middle rectal artery

A

Feeds rectum above pelvic diaphragm

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57
Q

Internal pudendal artery

A

Feeds distal rectum and vagina in perineum

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58
Q

Inferior rectal artery

A

Feeds rectum below pelvic diaphragm

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59
Q

Innervation of female reproductive organs

A

Ovaries, uterus, superior vagina innervated by autonomic nerve supply

Sympathetic T12-L2 to pelvic splanchnics

  • Synapse at pre-vertebral ganglia or abdominal aortic plexus –> travel with ovarian blood vessels to ovary
  • hypogastric/pelvic plexus to uterus and superior vagina

Parasympathetic pelvic splanchnics S2-S4

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60
Q

Distal vagina somatic nerve supply

A

Motor nerves and sensory innervation from pudendal nerve (S2-4)

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61
Q

What is a splanchnic nerve

A

splanchnic nerves are paired visceral nerves (nerves that contribute to the innervation of the internal organs), carrying fibers of the autonomic nervous system (visceral efferent fibers) as well as sensory fibers from the organs (visceral afferent fibers).

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62
Q

Visceral pain of the pelvic region

A

Uterine body above pelvic pain line - visceral pain travels with sympathetics to T12-L2 region

Uterine cervix and upper vagina below pelvic pain line - visceral pain travels with parasympathetic to S2-4

Low vagina travels with somatic pudendal nerve S2-4

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63
Q

Anesthesia blocks for the reproductive system

A

Spinal block - block lumbar splanchnic nerve (T12-L2), pelvic splanchnic nerve (S2-4) and pudendal nerve (S2-4) blocking all sensation from waist down

Caudal epidural block from pelvic splanchnic (S2-4) and pudendal nerve S2-4 results in loss of sensation of uterine cervix and vagina

Pudendal nerve block of pudendal nerve S2-4 results in loss of somatic sensation of vagina only

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64
Q

Lymphatic drainage of female reproductive system

A

Most lymph to back body wall to chyle cistern to thoracic duct

Lymph from distal vagina, labia majora and perineum drains superficially to superficial inguinal lymph nodes

Some parts of uterus associated with round ligament can drain to superficial inguinal lymph nodes

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65
Q

Branches of internal iliac artery supplying body wall

A

Middle sacral artery - midline sacrum, from aorta prior to bifurcation

Lateral sacral artery - feeds sacrum from lateral aspect

Iliolumbar artery - ascends on back body wall

Superior gluteal artery - leaves pelvis above the piriformis between lumbosacral trunk and S1

Inferior gluteal artery - leaves pelvis below piriformis

Internal pudendal artery - leaves pelvis, loops around pelvic diaphragm to access perineum

Obturator artery - travels with obturator nerve through obturator canal

Umbilical artery - obliterated artery that gives off superior vesicle artery prior to becoming occluded

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66
Q

Anterior branching of internal iliac from proximal to distal

A
  1. Superior vesicle artery
  2. Uterine artery
  3. Inferior vesicle/vaginal artery
  4. Middle rectal artery
  5. Internal pudendal artery (penetrates pelvic diaphragm to access perineum)
  6. Inferior rectal (can alternatively branch off internal pudendal artery)
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67
Q

Hypothalamus Pituitary Ovary Axis

A
  1. Hypothalamus secretes GnRH in pulsatilla manner
  2. GnRH stimulates anterior pituitary to secrete FSH and LH in pulsation fashion
  3. FSH and LH stimulate ovaries to produce estrogen and progesterone as well as ovulation
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68
Q

Affect of GnRH on LH or FSH secretion

A
  • amplitude and frequency of pulses determines predominant LH or FSH secretion by anterior pituitary
  • Follicular phase: GnRH pulses become faster to prepare for the future LH surge and high LH in literal phase
  • In literal phase pulses become slower to prepare for future high FSH in follicular
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69
Q

GnRH release regulation

A

3 negative feedback loops

  1. Long loop - estrogen and progesterone decrease release
  2. Short loop - FSH and LH decrease GnRH release
  3. Ultra short loop - GnRH inhibits its own release
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70
Q

Role of FSH

A

Targets granulosa cells in ovary causing follicular growth and estrogen production

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71
Q

Role of LH

A

LH surge stimulates ovulation

LH targets theca cells and corpus luteum

LH stimulate thecca cells to produce testosterone, which can be converted to estrogen by granulosa cells

LH stimulates corpus luteum to produce progesterone as well as estrogen

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72
Q

What’s the deal with estrogen and progesterone levels

A

Estrogen and progesterone are sex steroid hormone derived from cholesterol and produced in ovarian follicles

Estrogen level varies depending on stage of menstrual cycle
Low (<50) at menstruation
Increases with follicular development and peaks at 200
At end of literal phase, estrogen drops to menstrual levels

Progesterone level varies depending on stage of menstrual cycle
Low <2 before ovulation and high >5 after ovulation

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73
Q

Anatomy of the ovary

A

Enclosed in germinal epithelium

Outer cortex contains follicles, corpora lutes and corpora albicans

Inner medulla composed of connective tissue where blood vessels, lymph vessels and nerves enter the ovaries

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74
Q

Ovary functions

A
  1. Produce oocytes that are ovulated into Fallopian tube

2. Produce reproductive hormones including estrogen and progesterone

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75
Q

Sex hormone production pathway and where each sex hormone is produced

A

Cholesterol —> progesterone —> testosterone —> estrogen

Progesterone produced in all major ovarian cells (granulosa, theca, interstitial, corpus luteum)

Testosterone produced in theca, interstitial and corpus luteum

Estrogen produced by granulosa cells and corpus luteum

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76
Q

What is required to produce estrogen

A

Aromatase (lacking in the a cells)

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77
Q

Role of estrogen

A

Stimulate follicular development and onset of puberty

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78
Q

Main estrogen produced by ovary

A

Estradiol

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79
Q

Main estrogen produced by placenta

A

Estratriol

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80
Q

Main estrogen produced by adipose tissue

A

Estratone

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81
Q

What is the role of the estrogen to testosterone ratio in follicles

A

Determines the dominant follicle

Non-dominant follicles - inability to convert T to E leading to more androgen and follicular atresia

Dominant follicle - ability to convert

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82
Q

Regulation of FSH secretion

A
  1. Activism from granulosa cells stimulates FSH secretion
  2. Inhibin from granulosa cells inhibits FSH secretion
  3. Follistatin from granulosa cells neutralizes activism, thereby inhibiting FSH secretion
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83
Q

Oogenesis pathway

A

1) ovarian germ cells (oogonia) multiplies by mitosis until ~20 weeks gestation
2) at birth, oogonia (2n) enter meiosis I and arrest in prophase, becoming primary oocyte (2n) in a primordial follicle
3) at start of each menstrual cycle ~15-20 primordial follicles are recruited and develop into primary follicles, which is independent of FSH
4) during follicular phase, primary follicles develop into secondary, then one follicle will mature into tertiary follicle
5) before ovulation, LH surge allows primary oocyte (2n) to complete meiosis 1, becoming secondary oocyte (1n) that is halted in meiosis 2 metaphase plus 1st polar body 6) at ovulation, secondary oocyte (1n) exits ovaries and enters fallopian tubes
7) if ovulated secondary oocyte (1n) is fertilized with sperm, then secondary oocyte completes meiosis 2 to become an ovum, which joins sperm to form zygote

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84
Q

Menstrual cycle goal

A

goal of menstrual cycle is to produce a single, mature, fertilizable oocyte as well as provide right environment for it to implant and develop

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85
Q

Components/phases of menstrual cycle

A

2 cycles: ovarian and endometrial cycle

normal menstrual cycle usually 28 days

endometrial cycle

  1. day ~1-5 menstruation, part of proliferative phase
  2. day ~6-13 proliferative phase
  3. day 15-28 secretory phase

ovarian cycle

  1. day ~1-13 follicular phase 2. day ~14 ovulation
  2. day ~15-28 luteal phase

during menstrual cycle, female is fertile from ovulation day -3 days to ovulation +1 day
-3 days, because sperm can live in fallopian tube for 3 days
+1 day, because ovulated ovum is viable for ~1 day

length of follicular phase may vary, but length of luteal phase should be fixed at ~14 dayS

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86
Q

What occurs during the Follicular Stages

A

0) all follicles begin as primordial follicle
primordial follicle = oocyte surrounded by layer of flattened granulosa (follicular) cells
ovary start with all of its primordial follicles at birth, which then slowly depletes over time
primordial follicle contain a primary oocyte (2n) (primary oocyte are arrested at meiosis I prophase)

1) primordial follicles will develop into primary follicle, then secondary follicle
development from primordial follicle to secondary follicle is gonadotropin (LH & FSH) independent and occurs with time at any time, only a small portion of primordial follicles are developing to become primary follicle then secondary follicle
primary follicle result in:
- larger primary oocyte with a zona pellucida
- granulosa cells proliferating forming layers around oocyte
- interstitial cells close to growing follicles form the theca cells

2) under high FSH and high LH in follicular phase, a secondary follicle develops into tertiary (Graafian or astral or pre-ovulatory) follicle
high FSH stimulates many primary follicles to start development to secondary follicles
the fastest primary follicle that develops into secondary follicle at first becomes the dominant follicle
dominant follicle increase production of estrogen, that inhibit FSH, such that rest of the developing primary follicles die
non-dominant follicles also cannot convert testosterone into estrogen resulting in high testosterone that stimulates follicular atresia dominant follicle further increase estrogen that trigger LH surge
FSH stimulates proliferation, production of estrogen, increased FSH receptor and inhibin production in granulosa cells LH stimulates testosterone from theca cells, which then is converted to estrogen by granulosa cells
secondary follicle has
-formation of antrum, cumulus granulosa cells (surrounding oocyte) and mural granulosa cells (in the periphery)
-growth of granulosa and theca cell compartments
-increased vascularization of theca layer
-still a primary oocyte
FSH with high estrogen increase expression of LH receptor on granulosa cells, preparing the peripheral granulosa cells to become corpus luteum that is responsive to LH

3) LH surge result in ovulation
the high estrogen (>200) by dominant tertiary follicle cause LH surge
LH stimulates the primary oocyte (2n) to complete meiosis I to become a secondary oocyte (1n)
LH stimulates progesterone production by granulosa cells
LH surge results in ovulation of the tertiary oocyte into fallopian tube by increasing antral fluid and stimulating release of hydrolytic enzymes
the secondary oocyte with corona radiata granulosa cells are released into peritoneal cavity to be picked up into fallopian tube
the rest of follicle (peripheral granulosa and theca cell layers) remains in follicle and become vascularized with capillaries to become corpus luteum

4) corpus luteum forms and produce progesterone and estrogen in luteal phase corpus hemorrhagim -> corpus luteum -> corpus albicans
corpus luteum secretes progesterone and estrogen
corpus luteum contains large luteal cells (granulosa cell derived) and small luteal cells (theca cell derived) that produce progesterone and testosterone the high progesterone increases basal body temperature during luteal phase
corpus luteum is temporary (lasts 14 days) and will disintegrate into corpus albicans due to decline in LH
release of HCG from fertilization and implantation can rescue corpus luteum, which is them taken over by placenta after 4-5 months

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87
Q

What occurs during Endometrium stages

A

1) menstruation at day 0-5 due to low estrogen and progesterone progesterone withdrawal results in shedding of endometrium

2) proliferative phase at day 5-14 due to high estrogen
follicles produce high estrogen, which stimulate proliferation of endometrial cells increasing endometrial thickness

3) secretory phase at day 14-28 due to high progesterone
corpus luteum secrete high progesterone, which cause endometrial hypertrophy, thickening of spiral arteries and glycogen secretions from glands endometrium is thickest at secretory phase
the endometrium at secretory phase is optimal for implantation
endometrium most optimal for implantation about ovulation + 7 days

4) return to menstruation
disintegration of corpus luteum result in low estrogen and progesterone, causing endometrium to shed progesterone withdrawal is mainly responsible for normal menstrual bleeding

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88
Q

Mechanism of action of OCP

A

4 MOA by progesterone:

  1. Inhibiting ovulation (main mechanism)
  2. Change cervical mucous which blocks sperm
  3. Cause pseudo decidualization of endometrium to inhibit implantation
  4. Inhibit tubal peristalsis to inhibit fertilization
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89
Q

Role of estrogen in OCP

A

Estrogen does not contribute to mechanisms of contraception and is added to prevent breakthrough bleeding

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90
Q

OCP start methods

A

1) start on 1st Sunday after menses to have period free weekends
2) start on day 1 of that month
3) quick start ASAP (recommended)

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91
Q

Disadvantage to extending hormone days and/or shortening hormone free days with OCP

A

Can cause unscheduled bleeding

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92
Q

OCP schedule

A

Any change to traditional 21/7 regimen is reasonable as long as there is no more than 7 days without hormones

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93
Q

Absolute contraindications to OCP, ring and patch

A

smoker (>15 cigarettes / day) and over age 35

<6 weeks postpartum if breastfeeding

history of current or past venous thromboembolism (VTE)

current breast cancer

uncontrolled hypertension (diastolic >100 or systolic >160)

ischemic heart disease

complicated valvular heart disease

history of cerebral vascular accident (CVA) aka stroke

migraine headache with focal neurological symptoms

over age of 35 and migraine without aura (i.e. focal neurological symptoms)

diabetes with end organ involvement

severe cirrhosis, liver tumor, or active viral hepatitis

known thrombophilia

systemic lupus erythematous (SLE) with positive anti-phospholipid antibody (APLA)

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94
Q

False contraindication

A

OCP can be prescribed to anyone with family history of cancer

OCP can be prescribed without a pelvic exam

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95
Q

Benefits of OCP, ring and patch

A

Short term benefits

  • regulation of cycle
  • decreased bleeding
  • decreased dysmenorrhea, premenstual syndrome, acne, hirsutism

Long term benefit

  • decrease risk of endometrial and ovarian cancer
  • decrease risk of benign breast disease
  • decrease risk of colorectal cancer
  • decrease risk of acute PID and ectopic pregnancy
  • dec risk of ovarian cyst
  • amerliorate endometriosis
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96
Q

OCP, ring and patch contraceptive adverse effects

A

most women using OCP report no adverse effects
common adverse effects: headache, nausea, breast tenderness
usually mild, transient and self resolves in few months
less common adverse effects: decreased libido, unscheduled bleeding, mood changes
rare adverse effects: stroke, MI, VTE, increased risk of cervical cancer

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97
Q

Where should the contraceptive patch not be applied

A

Breast

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98
Q

When starting a new method of contraception what is the period duration where backup contraception should be used

A

7 days

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99
Q

Forgiveness period for contraceptive patch

A

2 days

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100
Q

Nuvaring forgiveness period

A

2 weeks

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101
Q

Progestin only pill mechanism of action

A

Thickening of cervical mucous to block sperm

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102
Q

Progestin only pill indication

A

When combined hormone contraceptive is contraindicated such as breastfeeding women, women with VTE

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103
Q

Use of progestin only pill

A

1 pill every day at same time (3 hour window) with no sugar pill week

Back up contracceptive x2 days if pill was taken late

Menstruation continues if baseline mensturation is regular

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104
Q

Progestin only adverse effects

A

Irregular bleeding

Worsening mood disorder such as depression

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105
Q

DMPA injectable progestin mechanism of action

A

1) inhibit ovulation
2) thickening of cervical mucus to block sperm
3) pseudo-decidualization (atophy) of endometrium that inhibit implantation

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106
Q

Use of injectable progestin DMPA

A

Intramuscular injection once every 3 months

breakthrough bleeding in first 3-6 months is normal, which usually can be treated with estrogen or NSAID, and can be ameliorated by shorter interval of injection

2 week forgiveness, where injection is still effective up to 14 weeks
if >14 weeks since last injection, do urine pregnancy test to rule out pregnancy, give injection and use back up contraception for 7 days

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107
Q

Absolute contraindication

A

known or suspected pregnancy (progesterone is not a teratogen, but pregnancy would make injectable progestin meaningless)

unexplained vaginal bleeding

current diagnosis of breast cancer

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108
Q

DMPA adverse effects

A

menstrual cycle disturbance including irregular non-stop bleeding or amenorrhea especially in first 3 months of use
after 1 year of use, ~50% develop amenorrhea
after 2 years of use, ~75% develop amenorrhea

weight gain due to increased appetite

decreased bone density

delay to fertility: return to fertility after 9 months on average post discontinuation of injectable progestin

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109
Q

Benefits DMPA

A

injectable progestin also used to treat menorrhagia, dysmenorrhea, endometriosis, chronic pelvic pain

menstrual suppression, inducing amenorrhea to treat menses-related symptoms, anemia and hygienic concerns

decrease risk of ovarian and endometrial cancer

decrease incidence of seizure

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110
Q

IUD contraindication

A 
known or suspected pregnancy
puerperal sepsis (infection and fever post childbirth or miscarriage)
immediate post septic abortion
current pelvic inflammatory disease, purulent cervicitis, chlamydia, gonorrhea
cervical or endometrial cancer
current breast cancer
unexplained vaginal bleeding
distorted uterine cavity anatomy
malignant trophoblastic disease
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111
Q

Adverse effects of IUD

A

unscheduled vaginal bleeding, which usually improve with time
LNG-IUS tend to decrease menstrual bleeding
copper IUD tend to increase menstrual bleeding
pain or dysmenorrhea
uterine perforation (0.1% risk)
infection (relative risk of 4 in first 3 weeks after insertion then return to normal baseline)
expulsion of device (5% of cases)
failure resulting in pregnancy, which may have increased risk of ectopic pregnancy
LNG-IUD cause hormonal side effects and functional ovarian cyst

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112
Q

What is the minimum beta hCG to see something in the uterus

A

1500

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113
Q

Copper IUD MOA

A

Main mechanism is prevention of fertilization

Other mechanisms:
foreign body reaction
endometrial change that adversely affects sperm transport
copper directly inhibits sperm motility and reduces sperm penetration through cervical mucous
inhibits implantation

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114
Q

Mirena (LNG-IUS) components

A

Progesterone

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115
Q

Mirena MOA

A

main mechanism of action is prevention of fertilization

other mechanisms of action include
thickening of cervical mucus by progesterone to block sperm
suppress endometrial estrogen and progestin receptor
inhibit ovulation by progesterone in some women
inhibit implantation
induce endometrial changes

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116
Q

LNG IUS indications

A

Contraception 3-5 years

Treat heavy menstrual bleeding

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117
Q

Male Vasectomy confirmation

A

need to use contraception for 3 months after operation and until 2 consecutive semen analysis confirms azospermia

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118
Q

What’s the deal with hysteroscopic tubal occlusion

A

insertion of alloy coil into fallopian tube via hysteroscope, which induce fibrosis and occlusion in Fallopian tube

need to do hysteosalpingography radiographic imaging to confirm tubal occlusion

must use contraception until occlusion is confirmed

complications include failure to successfully place, perforation of fallopian tube / uterus and expulsion of coil

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119
Q

Emergency contraception methods

A

Yuzpe method (estrogen + progesterone)

Plan B/Norlevo (Progestin only)

Copper IUD

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120
Q

Most effect emergency contraception method

A

Most effective emergency contraception (effective up to 7 days post unprotected sex exposure)

Then plan B then Yuzpe

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121
Q

Plan B/Norlevo components

A

Protesterone only

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122
Q

Plan B MOA

A

inhibit ovulation

change endometrium to inhibit implantation

disrupt luteal phase

effect on tubal transport time

however, does not disrupt an established pregnancy, so it is not effective with more time elapsed from sexual intercourse

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123
Q

Use of Plan B

A

earlier use increase effectiveness, best within 5 days of unprotected sexual intercourse

plan B have 2 tablets

both tablets at same time (preferred method) or one table followed by the other 12 hours later

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124
Q

Amenorrhea definition

A

absence of menstruation for at least 3 cyclic lengths

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125
Q

Oligomenorrhea definition

A

Cyclic length >35 days

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126
Q

Primary amenorrhea definition

A

failure to reach menarche (amenorrhea and no pubertal development by 14 years of age; or amenorrhea with secondary sexual characteristics by age 16)

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127
Q

Secondary amenorrhea definition

A

previously menstruating and cessation of menses (cessation of regular menses for 3 normal menstrual cycles or 6 months), typically in patient age <40

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128
Q

Major cause of amenorrhea

A

causes can be classified to physiologic, other endocrinopathies, medication, hypothalamus - pituitary - ovary - uterus - outflow tract
physiologic: pregnancy, breast feeding, menopause
other endocrinopathies: thyroid disease (hypothyroidism, hyperthyroidism), adrenal disease (adrenal insufficiency, adrenal hyperplasia), hyper-androgenism (congenital adrenal
hyperplasia, androgen secreting tumor), Cushing’s syndrome, constitutional delay of puberty
medication: contraception containing estrogen and / or progesterone, anti-depressants, anti-hypertensive, anti-psychotics, opiates
hypothalamus: hypothalamic tumor, functional suppression of hypothalamus, gonadotropin releasing hormone (GnRH) deficiency, infection (meningitis, TB, syphilis), traumatic
brain injury
functional suppression of hypothalamus-pituitary-varian axis due to physical stress on body including rapid weight loss, eating disorder, malabsorption, excessive
exercise, stress
pituitary: tumor (prolactinoma), empty sella syndrome, infiltrative disease (sarcoidosis), post-partum hypopituitarism (Sheehan syndrome)
ovary: polycystic ovary syndrome, ovarian insufficiency, ovarian insufficiency, ovarian tumor
ovarian insufficiency can be due to idiopathic causes, auto-immune destruction, chemotherapy, radiation, congenital causes (Turner’s syndrome, gonadal dysgenesis)
outflow tract obstruction: congenital (complete androgen resistance, imperforate hymen, Mullerian agenesis, transverse vaginal septum), acquired (Asherman syndrome, cervical
stenosis)

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129
Q

Amenorrhea history

A

HPI
menstruation history: onset of amenorrhea, previous menses if any (primary vs. secondary), previous menstrual cycle (length, pattern, consistency of pattern)
hypothalamus / pituitary tumor symptoms: headache, loss of vision, vomiting, galactorrhea
thyroid symptoms: temperature, heart rate, bowel movement
symptoms of androgen excess: acne, hirsutism, hair thinning, deepening of voice
primary ovarian insufficiency: vasomotor symptoms (hot flush, night sweats)
hyperandrogenism: acne, hirsutism
uterine or outflow tract obstruction symptoms: cyclic or acute pelvic pain
PMH
thyroid disease
surgery, radiation, chemotherapy
OB/GYN History
GTPAL
past sexually transmitted infections
OB/GYN surgery
Medication
contraception
dopamine antagonist including psychiatric medications
FH
age at menarche for mom and sisters
family history of genetic syndrome, autoimmune disease
SH
eating and exercise pattern
change in weight
sexual history

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130
Q

Amenorrhea physical exam

A

general: height, weight, BMI, inspection for dysmorphic feature (Turner’s syndrome)
Tanner staging
skin: inspect for hyperandrogenism (hirsutism, acne, male pattern hair loss), striae (Cushing’s syndrome)
head & neck: vision test (pituitary tumor), thyroid exam
abdomen: palpation for mass (ovarian or adrenal tumor)
genital: inspection for outflow tract obstruction, missing or malformed organ, thin vaginal mucosa (low estrogen), virilization (clitoral enlargement)

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131
Q

Amenorrhea investigations

A

blood work: CBC, b-hCG, LH, FSH, prolactin, TSH, serum estrodiol
pelvic ultrasound to rule out abnormal anatomy

Progesterone withdrawal challenge

Other: if estrogen not evidence from physical exam (normal vaginal discharge suggest normal estrogen level), then measure serum estradiol
if chronic disease suspected, CBC and metabolic panel
if history or physical exam suggest hyper-androgen, then serum testosterone
if Turner’s syndrome suspected, chromosome karyotype
if hypothalamus or pituitary cause suspected, then MRI head

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132
Q

Progesterone withdrawal challenge

A

not routinely done, because it can be substituted with estradiol (E2) to measure estrogen and pelvic ultrasound to measure outflow tract
progesterone for course of 10 days then stop to simulate luteal phase and see if bleeding ensues after withdrawal
withdrawal bleeding confirms adequate estrogen production and functional anatomy (responsive endometrium and patent outflow tract)
failure to bleed on progesterone withdrawal can be due to low estrogen from ovary, hypothalamic pituitary dysfunction, non-reactive endometrium, no uterus or anatomical
abnormality with uterine outflow tract
if failure to bleed, give estrogen then progesterone
failure to bleed with estrogen then progesterone confirms anatomic abnormality
bleeding with estrogen and progesterone confirms low estrogen, which need to be worked up to see if it is due to ovarian insufficiency or hypothalamic or pituitary disorder

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133
Q

Amenorrhea treatment

A

treatment always should address underlying cause
primary amenorrhea with no internal female reproductive organ usually have no viable treatment
pituitary dysfunction: symptom relief with estrogen and progesterone replacement (e.g. oral contraceptive pill), LH & FSH injection for fertility
hypothalamus dysfunction: if functional hypothalamic suppression, then need to correct underlying cause, otherwise symptom relief with estrogen and progesterone replacement
pituitary or hypothalamus tumor: consider surgical resection, LH & FSH injection for fertility
ovarian dysfunction: symptom relief with estrogen and progesterone replacement (e.g. oral contraceptive pill), egg donor and in-vitro fertilization for fertility
obstructive tract should be treated with surgical repair
other endocrinopathy: address and treat endocrinopathy (e.g. thyroid replacement for hypothyroidism)

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134
Q

Primary amenorrhea top differential diagnoses

A

Chromosomal abnormalities leading to primary ovarian insufficiency - Turner’s syndrome, Fragile X syndrome

Other genetic conditions - androgen insensitivity, congenital adrenal hyperplasia

Anatomic abnormalities - Mullerian agenesis

Constitutional delay

Primary amenorrhea with normal breast development - androgen insensitivity syndrome, Mullerian agenesis, Mullerian uterine septum

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135
Q

Pathophysiology amenorrhea due to Turner’s syndrome

A

45 X lacking 1 X chromosome

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136
Q

Pathophysiology amenorrhea due to fragile X syndrome

A

abnormal X chromosome

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137
Q

Androgen insensitivity

A

46XY karyotype with androgen receptor defect leading to female external genitalia, no uterus, no cervix, no fallopian tube, little hair growth

Normal functioning testes secreting normal male testosterone

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138
Q

Pathophysiology amenorrhea due to congenital adrenal hyperplasia

A

Excessive androgen production leading to anovulation

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139
Q

Pathophysiology amenorrhea due to Mullerian agenesis

A

46XX karyotype, female phenotype, no uterus, no cervix, no fallopian tube

Normal ovaries

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140
Q

Approach to primary amenorrhea

A
  1. History and physical
    Growth curve, wrist xray for bone age
    If normal growth and delayed wrist xray with normal work up then constitutional delay
  2. TSH - fu with thyroid hormone
    Prolactin - MRI of head
    bhCG
  3. Further tests depend on presence of uterus on u/s
    - No uterus suggests genetic syndrome (fu with karyotype and testosterone)
    46XX with female range testosterone is Mullerian agenesis
    46XY with male range testosterone is androgen insensitivity
    - Normal uterus base diagnosis on FSH level
    High FSH suggests primary ovarian insufficiency (repeat in 1 month to diagnose with POI, order karyotype to evaluate Turner or presence of Y chromatin, test for fragile X)
    Low FSH can be physiologic (functional amenorrhea, constitutional delay) or pathologic (MRI) hypothalamus pituitary disorder
    Normal FSH can be due to ovarian tumour, adrenal tumour or congenital adrenal hyperplasia - High 17-OH-progesterone =CAH
    - High testosterone =u/s for ovarian tumour
    - High DHEAS = adrenal imaging for tumour
    - Normal testosterone and DHEA consider PCOS
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141
Q

How do adrenal tumours cause amenorrhea

A

Glucocorticoid secreting tumours likely secrete cortisol, which suppresses GnRH production

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142
Q

Secondary amenorrhea top differential

A

Hypothalamic - eating disorder, stress

Pituitary - prolactinoma

Thyroid - hypothyroidism

Ovary - PCOS, POI

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143
Q

Approach to secondary amenorrhea

A
  1. History and physical - review medications including contraceptive and illicit drugs
  2. TSH (thyroid hormone if abnormal), prolactin (MRI if abnormal)
  3. Further tests depend on level of FSH
    a) high FSH suggests POI
    Repeat in 1 month, measure serum estradiol, order karyotype to rule out Turner’s syndrome
    b) Normal or low FSH/LH
    Functional amenorrhea
    MRI head to rule out hypothalamus/pituitary abnormality if h/a, vomiting, vision changes
    Hx OB/GYN procedure do withdrawal bleed or hysteroscopy to evaluate for Asherman’s syndrome
    Signs of hyperandrogenism (virilization such as hirsutism, acne, hair thinning, enlarged clitoris) - order serum testosterone (high PCOS, very high or rapid onset imaging for adrenal and ovarian tumour), DHEA-S and 17-hydroxyprogesterone (CAH if very high)
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144
Q

Ovarian insufficiency is associated with

A

other autoimmune diseases

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145
Q

Ovarian insufficiency causes

A

90% are idiopathic

Chromosomal abnormalities

Environmental insult (chemo, radiation, infection, surgery)

Tumour

Empty sella syndrome

Autoimmune

Infiltrative process

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146
Q

Ovarian insufficiency pathophysiology

A

Inadequate follicles to sustain menses due to failure to form enough primordial follicles or accelerated loss of follicles or damage to follicle by autoimmunity or toxins

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147
Q

Ovarian insufficiency clinical presentation

A

Primary or secondary amenorrhea

Menses with cycle interval >90 days

Oligo-menorrhea (<9 cycles per year)

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148
Q

Investigations in ovarian insufficiency

A

Normal TSH, prolactin

Can have normal anatomy on ultrasound

Consistently high FSH and LH

Consistently low estradiol

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149
Q

Ovarian insufficiency diagnosis

A

Patient diagnosed with POI if patient meets all of criteria:

  1. Primary or secondary amenorrhea for 3 months or change from regular menstruation for 3 months
  2. High FSH>40 on 2 occasions a month apart
  3. Age <40
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150
Q

POI complications

A

Leads to low estrogen, resulting in increased risk of osteoporosis as well as atherosclerosis and its consequent cardiovascular diseases

POI lead to infertility

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151
Q

POI management

A
  1. Pre-pubertal POI
    - slowly increasing estrogen for 2 years or until breakthrough bleeding
    - then add progesterone to induce cyclic withdrawal bleed
  2. Post puberty POI
    Hormone therapy of estrogen for day 1-26 of menstrual cycle and progesterone for day 14-26 (OCP, patch, ring, copper + hormone replacement therapy, IUS + estrogen replacement therapy)

weight bearing exercise and calcium and vitamin D supplement to prevent osteoposrosis

BP, lipid monitoring to assess cardiovascular disease risk + diet, no smoking, exercise
Psychosocial support for patient to deal with infertility, but recommend contraceptive if not wanting to conceive because there is still 5% chance of spontaneous pregnancy
Consider egg/embryo donor or adoption if patient wants children

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152
Q

What is the purpose of estrogen replacement in post puberty POI

A

Prevent osteoporosis, CVD, vasomotor symptoms

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153
Q

Normal and abnormal duration menstruation

A

4-7 days

<2 days and >7 days is abnormal

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154
Q

Normal and abnormal volume menstrual flow

A

30 mL

>80 mL is abnormal

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155
Q

Normal and abnormal length of menstrual cycle

A

24-35 days is normal

<24 or >35 days is abnormal

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156
Q

Menorrhagia

A

regular normal interval with excessive volume >80mL and / or duration of flow (i.e. heavy menstrual bleeding) >7 days

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157
Q

Metrorrhagia

A

irregular intervals with normal or reduced volume and duration of flow (i.e. irregular menstrual bleeding)

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158
Q

Menometrorrhagia

A

irregular intervals and excessive volume and duration of flow (i.e. irregular heavy menstrual bleeding)

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159
Q

Polymenorrhea

A

cyclic length <24 days

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160
Q

Types of AUB

A 
Menorrhagia 
Metrorrhagia 
Menometrorrhagia 
Polymenorrhea 
Post-menopausal bleeding 
Amenorrhea 
Oligomenorrhea
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161
Q

Dysmenorrhea

A

Pain with menstruation

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162
Q

What are some conditions that could mimic AUB

A

Vaginal bleeding
Hematuria
Hematochezia

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163
Q

AUB differential diagnosis during reproductive years

A
    • Pregnancy and its complications
  • Functional- Blood dyscrasia, hypothyroidism, luteal dysfunction
  • Pathological (PALM COEIN)
164
Q

Pathological causes of AUB for women in reproductive years

A

PALM - structural abnormalities

Polyps 
Adenomyosis 
Leiomyoma (ie fibroids) 
Malignancy 
Hyperplasia

Malignancy or hyperplasia = endometrial cancer, endometrial hyperplasia, cervical cancer

COEIN are non-structural abnormalities
Coagulopathy
Ovulatory dysfunction - all differential diagnosis for oligomenorrhea and amenorrhea
Endometrial dysfunction - endometrial hemostasis disorder, endometritis, abnormal local inflammatory response, abnormal vasculogenesis of endometrium
Iatrogenic - medications, IUD
Not yet classified (ie idiopathic)

165
Q

Medications that can cause AUB in reproductive years

A

Hormone medication - androgen, estrogen, progesterone
Hormone related therapy medication - GnRH agonist, aromatase inhibitor, SERM, SPRM

Other medications: SSRI, TCA, anti-psychotics, corticosteroids, anti-platelet agents, anti-coagulants

166
Q

How do structural abnormalities causing AUB generally present

A

(PALM)

Inter menstrual bleeding

167
Q

Anovulatory or ovulatory AUB?

a) coagulopathy
b) iatrogenic
c) ovulatory dysfunction
d) endometrial dysfunction

A

a) either
b) either
c) anovulatory
d) ovulatory

168
Q

Anovulatory AUB presentation

A

Unpredictable and irregular menstrual cycle with prolonged or heavy bleeding

169
Q

Ovulatory AUB presentation

A

Predictable and cyclic menses with normal duration

170
Q

Top things on differential for post-coital bleeding

A

Cervical dysplasia

Polyp

171
Q

Approach to AUB in Pre-menopausal women

A
  1. Confirm uterus as source of bleeding
  2. Rule out pregnancy
  3. Rule out coagulopathy, ovulatory dysfunction, iatrogenic of COEIN
  4. Rule out structural causes (PALM) with TVUS, saline infusion sonography and hysteroscopy
  5. Determine if ovulatory or anovulatory based on history
    Anovulatory consider endocrinopathy and follow route for oligomenorrhea/amenorrhea
    Ovulatory consider endometrial dysfunction (workup with hysteroscopy and endometrial biopsy)
172
Q

Approach to AUB in post-menopausal women

A

AUB in post-menopausal women is malignancy, likely endometrial cancer until proven otherwise

1) rule out cause due to medication including hormone replacement
2) rule out structural causes with endometrial biopsy, trans-vaginal ultrasound / saline infusion sonography and hysteroscopy
3) consider neoplasia elsewhere in vagina, cervix, fallopian tube, bladder / urethra and rectum
4) based on exclusion (no findings in previous steps), diagnose with post-menopausal AUB most likely due to endometrial / vaginal atrophy

173
Q

General medication management for AUB

A

Medication is 1st line therapy if non-structural abnormality

Non-hormonal and/or hormonal for regular menorrhagia

Hormonal for irregular menorrhagia

174
Q

Non-hormonal treatment of AUB

A
  1. Iron supplement
    Indication - iron deficient anemia
  2. NSAID
    MOA - decrease blood loss by vasoconstriction
    Indication - menorrhagia, pain relief for dysmenorrhea
    Less effective than other forms of therapy
  3. Anti-fibrinolytics TXA
    MOA - inhibit plasminogen activator to decrease bleeding
    Indication - menorrhagia
    Contraindication - thromboembolism (DVT, PE)
    Side effects - nausea, GI upset, leg cramps, retinal vascular occlusion
175
Q

Hormonal treatment AUB

A
  1. Combined hormone (estrogen progestin) contraceptive
    Indication - menorrhagia (regular or irregular), irregular menstrual cycle
    Most prescribed treatment for AUB
    MOA - progestin suppress ovulation and estrogen to support endometrium preventing breakthrough bleeding thereby decreasing blood loss (also regulate cycle, contraception, prevent hyperplasia and treat dysmenorrhea)
    Contraindication - heavy smoking, DVT, stroke, uncontrolled hypertension, migraine with neurological symptom, breast cancer, CAD, liver disease
  2. Progestin (oral, injection, IUS)
    Indication - irregular menstrual cycle, menorrhagia (irregular or regular)
    MOA - progestin inhibits ovarian steroid synthesis causing endometrial atrophy, decreasing blood loss, cyclical withdrawal can induce endometrial shedding
    Oral progestin is not effective for regualr menorrhagia and less effective than NSAID and TXA
    IUS decrease menstrual blood loss and decrease frequency of period, which is more effective than other progestin treatment and can treat dysmenorrhea
  3. GnRH agonist (Lupron)
    Indication - menorrhagia (regular or irregular), shrinkage of fibroid, dysmenorrhea
    MOA: induce reversible menopause by inducing endometrial atrophy and amenorrhea
    Side effects - menopausal symptoms (hot flash, mood fluctuation, vaginal dryness, bone effects)
176
Q

Surgical management of AUB

A

Non structural - endometrial ablation or hysterectomy (definitive treatment)

Structural abnormality - specific surgical management

177
Q

Medications that can cause vaginal bleeding

A

Contraception - hormone contraceptives, IUD

Post menopausal hormone therapy

Tamoxifen

Anti-coagulants

Corticosteroids

Chemotherapy

Phenytoin

Antipsychotic drugs

178
Q

Life threatening causes of vaginal bleeding

A

Early pregnancy - ruptured ectopic, spontaneous abortion

Late pregnancy - placental abruption, placenta previa

Post-partum - PPH

Ovary - ruptured ovarian cyst - ovarian torsion

Uterus - acute severe menorrhagia

Trauma to genital tract, foreign body in genital trat

Infection to genital tract including PID, salpingitis

Gynecologic malignancies

179
Q

Approach to vaginal bleeding

A
  1. Stabilize patient
  2. Rule out pregnancy
  3. Rule out bleeding source outside genital tract (urinary, GI)
  4. Rule out vulva, vagina, cervix causes on physical exam
  5. Consider ovarian, fallopian tube and uterus causes
180
Q

Gynecologic emergencies that present with acute pelvic pain

A

Ectopic pregnanc

Ruptured ovarian cyst

Ovarian torsion

PID

181
Q

What is the Ring of Fire sign indicative of on ultrasound

A

The ring of fire sign, also known as ring of vascularity, signifies a hypervascular lesion with peripheral vascularity on color or pulsed Doppler examination of the adnexa due to low impedance high diastolic flow 1.

This sign can be seen in:

corpus luteum cyst (more commonly)
ectopic pregnancy

182
Q

What is the double sac sign indicative of on ultrasound

A

The double decidual sac sign (DDSS) is a useful feature on early pregnancy ultrasound to confirm an early intrauterine pregnancy (IUP) when the yolk sac or embryo is still not visualized. It consists of the decidua parietalis (lining the uterine cavity) and decidua capsularis (lining the gestational sac) and is seen as two concentric rings surrounding an anechoic gestational sac. Where the two adhere is the decidua basalis, and is the site of future placental formation.

183
Q

What may be seen on ultrasound if a ruptured ovarian cyst is present

A

Ovarian cyst (thin wall, posterior acoustic enhancement, no blood flow)

Fluid in pouch of Douglas or Morrison’s pouch or LUQ

184
Q

What is the Pouch of Douglas

A

An extension of the peritoneal cavity between the rectum and the back wall of the uterus. Also known as the rectouterine pouch

185
Q

What is Morrison’s pouch

A

The hepatorenal recess (subhepatic recess, pouch of Morison or Morison’s pouch) is the space that separates the liver from the right kidney

186
Q

What might you see on imaging with Ovarian Torsion

A

Enlarged ovary, ovarian mass, multiple small peripheral follicles (often in context of adnexal mass)

Abnormal ovarian location

Decreased/no Doppler flow in ovary

187
Q

Ovarian torsion management

A

Immediate surgery to detorse viable ovary

Otherwise salpingoophorectomy for non-viable ovary

188
Q

PID pathophysiology

A

Infection of upper genital tract structure (uterus, Fallopian tube, ovaries) by STI (commonly Gonorrhea or Chlamydia), which may cause endometritis, salpingitis, oophoritis, tubo-ovarian abscess, peritonitis, peri-hepatitis

189
Q

PID clinical presentation

A

Pelvic pain (classifcally during or shortly after menses)

Vaginal discharge or bleeding

Dysuria

Fever, chills

190
Q

PID management

A

Antibiotic therapy (ex. Ceftriaxone 250 mg IM single dose + Doxycycline 100 mg PO BID x 14 days)

191
Q

Chronic pelvic pain definition

A

Pelvic pain below umbilicus for >6 months duration, which causes functional disability or requiring treatment

192
Q

Risk factors of chronic pelvic pain

A

History of previous sexual abuse or assault in 20%

193
Q

Red flags on hx and PE for chronic pelvic pain

A
  1. Constitutional symptoms
  2. GI symptoms - hematochezia
  3. ObGyn symptoms - peri menopausal irregular vaginal bleeding, post menopausal vaginal bleeding, post coital bleeding
194
Q

Investigations for chronic pelvic pain

A

Blood work - beta-hCG (repeat in 48 h if positive), CBC, ESR

Vaginal swab for STI

Urinalysis r&M C&S for UTI or renal calculus

195
Q

Chronic pelvic pain syndromes

A
  1. Pelvic pain dysfunction/chronic pelvic pain syndrome
  2. Vestibulitis vulvodynia syndrome
  3. Pelvic congestion syndrome
196
Q

Pathophysiology of pelvic pain dysfunction/chronic pelvic pain syndrome

A

Idiopathic spasm of pelvic floor muscles (elevator ani)

197
Q

Pelvic pain dysfunction/chronic pelvic pain syndrome symptoms

A

Pelvic pain out of proportion to pathology, dyspareunia, vaginismus (spasm of vagina), dysuria, dyschezia, pain elsewhere (back, lower abdomen, groin, leg)

198
Q

Impact of pelvic pain dysfunction/chronic pelvic pain syndrome

A

Impaired function at home/work

Decreased libido -> decreased sexual activity

199
Q

Signs of pelvic pain dysfunction/chronic pelvic pain syndrome

A

Tight, tender, band-like muscle in vagina and rectum

200
Q

Symptoms Vestibulitis vulvodynia syndrome

A

Vulvar discomfort or pain

Dyspareunia (superficial —> deep)

Perineal burning or rawness

Urinary symptoms (urgency, frequency, dysuria)

201
Q

Vestibulitis vulvodynia syndrome Signs

A

Erythema of Bartholine openings and hymen

Tenderness on q tip probe into vestibule, vaginismus and pelvic pain dysfunction

202
Q

Pelvic congestion syndrome Risk factors

A

Multiparity

Sedentary lifestyle

Constipation

Sexual dissatisfaction

203
Q

Pelvic congestion syndrome Pathophysiology

A

Pelvic vein varicosities

204
Q

Pelvic congestion syndrome Symptoms

A

Dull aching pain in pelvis and lower abdomen aggravated by standing and relieved with lying down

May progress to dyspareunia, dysmenorrhea, back pain, vaginal discharge

205
Q

Pelvic congestion syndrome Investigations

A

Us showing pelvic veinvaricosities

206
Q

Non specific treatment of chronic pelvic pain

A

Medication -
Acetaminophen, NSAID, opioids
If cyclic consider combined OCP, progesterone oral, IM or IUS, GnRH agonist (Lupron), Danazol
If non-cyclic consider gabapentin or amitriptyline

Surgery - laparoscopy, lysis of severe adhesions, total abdominal hysterectomy for failed medical treatment

207
Q

Special cases for pap tests

A
  1. Patients previously treated for cervical dysplasia - annual screening
  2. Immune compromised - annual screening
  3. Total hyserectomy including cervix for benign disease - none
  4. Visual cervical abnormality on speculum exam or abnormal symptoms - colposcopy regardless of pap test cytology findings
208
Q

LSIL

A

Low grade squamous intraepithelial lesion
Minor dysplasia not likely to become cancer, probably due to HPV infecion
Equivalent to cervical intraepithelial neoplasia (CIN 1)

209
Q

HSIL

A

High grade squamous intraepithelial lesion
Severe dysplasia that is more likely to progress to cancer
Equivalent to CIN 2 or 3

210
Q

Glandular cell abnormalities

A

AGC - atypical glandular cells

AIS - adenocarcinoma in situ

211
Q

ASCUS for patient age <30 follow up

A

repeat Pap test cytology every 6 months x 2

if any of the Pap tests cytology every 6 months is abnormal (i.e. >ASCUS), then colposcopy

if both Pap tests cytology every 6 months are negative, then return to routine screening every 3 years

212
Q

ASCUS for patient age >30 with HPV testing available follow up

A

A) HPV testing available
1) HPV testing
if HPV testing is negative, then proceed to 2
if HPV testing is positive, then colposcopy

2) Repeat Pap test cytology in 1 year
if repeat Pap test cytology is abnormal (i.e. >ASCUS), then colposcopy
if repeat Pap test cytology is negative, then return to routine screening every 3 years

B) HPV testing not avaiable
follow same algorithm as ASCUS for patient age <30 with repeat Pap test cytology every 6 months x 2

213
Q

LSIL follow up

A

straight to colposcopy or follow same algorithm as ASCUS for patient age <30 with repeat Pap test cytology every 6 months x 2
HSIL: straight to colposcopy
ASC-H: straight to colposcopy
AGC: straight to colposcopy

214
Q

HSIL

A

straight to colpo

215
Q

ASC-H

A

straight to colpo

216
Q

AGC

A

straight to colpo

217
Q

Satisfactory colposcopy

A

Only when transformation zone between stratified squamous epithelium and glandular epithelium is visualized

type 1 transformation zone = entire transformation zone visualized on colposcopy
type 2 transformation zone = entire transformation zone fully visualized when cervix is opened
type 3 transition zone = entire transformation zone is not visualized even when cervix is opened

type 1 and 2 transformation zone is satisfactory
type 3 transformation zone is not satisfactory

218
Q

What is the cervical intraepitheliual neoplasia system

A

colposcopy biopsy classified by cervical intraepithelial neoplasia system (CIN 1, 2 and 3), which signify premalignant transformation and dysplasia that is not cancer but may progress
to cancer

219
Q

What to biopsy during colposcopy

A

if any abnormal appearing tissue such as abnormal vascular pattern, mosiacism, punctate lesion, nodular lesion or turns white with acetic acid on colposcopy, then biopsy
if no abnormal lesion identified, then biopsy transition zone

220
Q

Management post colpo < CIN1

A

if biopsy is less than CIN 1, then return to screening protocol (Pap test very 3 years)

221
Q

What is an excisional biopsy

A

excisional biopsy mentioned above can be loop electrosurgical excision (LEEP), laser, cryotherapy or cone biopsy

222
Q

Management post colpo CIN 2 or 3

A

CIN 2 or 3 have risk of cancer

CIN 2 or 3 usually treated with excisional biopsy

223
Q

Management post colpo CIN 1

A

CIN 1 biopsy rarely progress to cancer
a) if satisfactory (type 1 or 2 transformation zone) colposcopy, then observe with pap test at 12 months and then manage according to cytology
b) if unsatisfactory (type 3 transformation zone) colposcopy, then observe with pap test and colposcopy at 6 months and 12 months
i) if colposcopy and pap test at both visits are negative for CIN, then return to screening protocol
ii) if CIN persist or progress, then treat by ablation
c) if CIN 1 after HSIL or AGC on pap test, then review biopsy histology with pap test cytology
if discrepancy, then excisional biopsy

224
Q

Management post unsatisfactory colpo

A

if unsatisfactory (type 3 transformation zone) colposcopy and cytology was AGC or HSIL, then diagnostic excisional biopsy with LEEP or cone biopsy with endocervical curretage

225
Q

STIs tested for with vaginal culture and microscopy

A

Yeast

Bacterial vaginosis

Trichomoniasis

226
Q

STIs tested for with cervical culture

A

Chlamydia

Gonorrhea

227
Q

STIs tested for with blood work

A

HIV

Hepatitis B - HBSAg

Hepatitis C - HCV RNA testing

Syphilis - VDRL

228
Q

When to perform bloodwork testing for STIs

A

Can perform immediately, but HIV, Hep B and Hep C have a latency period so need to repeat bw at 3 and 6 months

229
Q

STI Urine testing

A

Urine PCR for chlamydia and gonorrhea
b-hCG

No voiding for 2h then beginning of ‘dirty’ urine (20mL)

230
Q

Herpes testing

A

Open intact vesicle with needle, then culture liquid with special swab with liquid virus transport

Send to lab within hours

231
Q

HPV diagnosis

A

Diagnosed clinically based on warts on clinical exam

232
Q

HPV testing indication

A

Testing for triage of ASCUS pap test for patient 30+ years

233
Q

HPV testing technique

A

concomitant with cervical pap test with Dacron swab or cervical brush

234
Q

STI pharynx testing

A

Gonorrhea

Insertion of regular swab and rub against posterior pharynx and tonsillar crypts

235
Q

Rectum STI testing

A

Testing for gonorrhea and chlamydia

Insertion of regular swab 2-3 cm into anal canal pressing laterally to avoid feces

Need to repeat and obtain another specimen if visible fecal contamination

236
Q

Urethra STI testing

A

Testing for gonorrhea and chlamydia

no voiding for 2 hours then regular swab moistened with water inserted 1-2 cm up female urethra and 3-4 cm up male urethra

237
Q

Vulvovaginitis pathophysiology

A

inflammation of vulva and/or vagina

238
Q

Vulvovaginitis clinical presentation

A

vaginal discharge

vulvo-vaginal pruritus

vulvovaginal pain

239
Q

most common cause of Vulvovaginitis

A

infection (BV, vaginal candidiasis, trichomoniasis)

240
Q

How does vaginal discharge vary throughout the menstrual cycle

A

Low estrogen in follicular phase results in thick and sticky vaginal discharge

high estrogen in luteal phase results in clearer, wetter and more stretchy vaginal discharge, which is more conducive to sperm travelling

241
Q

BV epidemiology

A

Most common cause of abnormal vaginal discharge

Increases risk of acquiring STIs

242
Q

BV risk factors

A

African American

Changing sex partner, lesbian partner with BV, douching

Change to vaginal environment: IUD, antibiotic use, co-existing STI

243
Q

BV pathophysiolgy

A

normal flora in vagina includes Lactobacillus, which produce hydrogen peroxide to prevent multiplication of other vaginal microorganism

bacterial vaginosis is not an infection, but polymicrobial replacement of normal flora and multiplication in vagina without inflammation

polymicrobial includes anaerobes (Prevotella, Mobiluncus, Bacteroides), Gardrerella, Ureaplasma and Mycoplasma

244
Q

BV presentation

A

most asymptomatic

increased thin, white and homogeneous vaginal discharge with a foul odor

245
Q

BV investigations

A

Whiff test - fishy odor when alkali (10% KOH) is added to a wet mount containing vaginal discharge

pH >4.5 (normal 4)

Miscroscopy of wet mount containing vaginal discharge - clue cells (vaginal squamous epithelial cells coated with bateria around its edges)

246
Q

BV diagnosis

A

Amsel’s criteria - 3/4 of following

  1. Thin white homogeneous vaginal discharge
  2. pH >4.5
  3. Positive Whiff test
  4. Clue cells on microscopy
247
Q

BV treatment

A

Treat only if symptomatic

Treat with antibiotics (oral better than topical)
1st line - Metronidazole 500 mg PO BID x 7 days
2nd line - Metronidazole gel or Clindamycin cream

If pregnant treat with metronidazole oral or clindamycin oral

testing and treating sexual partner not recommended

248
Q

Vulvovaginal Candidiasis (VVC) epidemiology

A

2nd most common vaginal infection after BV

249
Q

Vulvovaginal Candidiasis (VVC) risk factors

A

change in vagina microbiological environment: uncontrolled diabetes, systemic antibiotic use

immunocompromised state

high estrogen level: pregnancy, obesity, oral contraceptive pill (OCP)

low estrogen (menopause, pre-puberty) decreases risk of VVC

250
Q

VVC pathogenesis

A

candida yeast is part of normal vaginal flora, where overgrowth can cause symptoms under changed vagina environment
infection of vagina and vulva by candida fungal species
95% cases are candida albicans, which respond well to usualy therapies
less common infections by non-albicans candida species which is harder to treat: candida glabrata (torulopsis), candida parapsilosis, candida krusei, saccaromyces cerevisiae

251
Q

VVC clinical presentation

A

vaginal symptoms: thick white clumpy “curdy and cottage cheese like” vaginal discharge which is usually odorless

skin symptoms: vulval itch, burning, pain or soreness; skin fissures, erythema, edema or satellite lesions (sores in surrounding skin) of vulva

252
Q

VVC investigations

A

pH litmus paper test in vagina: pH usually within normal range and <4.5 (normal vaginal pH is ~4)
vaginal swab KOH wet mount / culture: yeast with hyphae and spores

253
Q

VVC diagnosis

A

diagnosis by microbial culture of vaginal swab showing Candida (bud + hyphae) plus symptoms of vulvovaginitis

254
Q

VVC treatment

A

treat only if symptomatic

oral antifungal: Fluconazole 150mg PO in single dose

topical antifungals: azoles (Clotrimazole, Miconazole, Terconazole) suppository or cream for 3 days if uncomplicated cases; 7 days if complicated cases (diabetes,
immunocompromised, atypical Candida)

oral is preferred over topical treatment for women except when pregnant
only topical treatment is recommended for pregnant women

if resistant to azoles or atypical (not Candida albicans), then topical boric acid powder

gentian violet is effective
other alternatives treatments are not effective including Lactobacillus, probiotics, garlic tampons, tea tree oil, echinacea, golden seal, yeast guard suppositories

255
Q

Trichomoniasis pathogenesis

A

trichomoniasis is a disease caused by trichomonas vaginalis, a unicellular flagellated parasite motile protozoa

transmission by genital sexual contact, which is reduced by condom

trichomonas can infect vagina, bladder or urethra

256
Q

Trichomoniasis clinical presentation

A

50% of women are asymptomatic

onset of symptoms usually 1 week after contact

vagina symptoms: yellow-green malodorous diffuse frothy vaginal discharge, pruritus, dyspareunia

urinary symptoms: dysuria, increased urinary frequency

complication: rarely may cause pelvic inflammatory disease

257
Q

Trichomoniasis on physical exam

A

vaginal discharge

strawberry cervix (petechiae) due to punctate hemorrhage

258
Q

Trichomoniasis investigation

A

Microscopy of vaginal swab - motile flagellated organism, many WBC, inflammatory cells (PMNs)

259
Q

Trichomoniasis diagnosis

A

trichomoniasis diagnosed by trichomonas visualized on microscopy of vaginal swab sample

260
Q

Trichomoniasis management

A

not a reportable disease
treat even if asymptomatic
oral antibiotic therapy: Metronidazole 2g PO single dose or 500mg PO BID x 7 days
sexual partners should also be treated

261
Q

Post menopasual atrophic vaginitis pathogenesis

A

post menopausal women have low estrogen, leading to atrophy of vagina
atrophy of vagina usually only lead to vaginal dryness, but can cause an inflammation within the vagina resulting in vaginal discharge

262
Q

Post menopasual atrophic vaginitis clinical presentation

A

vagina symptoms: yellowish vaginal discharge, feeling of dry and irritated vagina despite discharge, dyspareunia, pruritus, itching, burning, may cause vaginal bleeding

speculum exam: vaginal petechiae

263
Q

Post menopasual atrophic vaginitis treatment

A

vaginal estrogen (ring, tablet or cream) is most effective, which need to be applied for life and achieves full effect in 3 months

systemic estrogen is less effective than vaginal estrogen with more side effects and contraindications

264
Q

Hirsutism definition

A

excessive male-pattern hair growth in women

265
Q

Virilization definition and presentation

A

excessive development of exaggerated masculine characteristics in women

usually presenting with clitoromegaly, deepening of voice, acne, hirsutism, baldness, increased muscularity

266
Q

Pathophysiology of hirsutism and virilization

A

hirsutism and virilization are caused by excess androgen secretion (hyper-androgenemia) including testosterone and dihydrotestosterone (DHT)

usually high androgen level results in hirsutism first, and very high androgen level results in virilization

excess androgen may be from ovary, adrenal gland or exogenous source

ovary secrete testosterone and androstenedione

adrenal gland secrete dehydroepiandrosterone sulfate (DHEA-S) and androstenedione

267
Q

Hirsutism and virulization differential diagnosis

A

1) Pituitary
a) Cushing’s disease, resulting in increased ACTH that stimulate secretion of adrenal androgen
b) acromegaly

2) Excess Androgen from Adrenal Gland
a) neoplasm: androgen secreting adrenal tumors
b) genetic: 21-hydroxylase deficiency (aka congenital adrenal hyperplasia), which stop synthesis pathway of mineral-corticoid and glucocorticoid, resulting in excess precursor converted to androgen

3) Excess Androgen from Ovary
a) polycystic ovarian syndrome (PCOS)
b) ovary hyperthecosis
c) androgen secreting ovarian tumors: Sertoli-Leydig cell, Granulosa-theca cell, Hilus cell

4) Exogenous
a) exogenous androgens: testosterone, DHEA

5) Other
a) pregnancy due to luteoma or theca-lutein cyst
b) severe insulin resistance syndromes
c) idiopathic hirsutism

268
Q

Clinical presentation of excess androgen

A

hirsutism: excess terminal hair growth (dark coarse hair) in androgen dependent area (upper lip, chin, mid-sternum, upper abdomen, back, buttocks)

hirsutism can be graded based on Ferriman-Gallwey score, which grade 9 androgen dependent body areas from 0 (no hair) to 4 (frankly virile)

hirsutism defined as >8 for black or white women, >2 for Asian women, >9-10 for Mediterranean, Hispanic and Middle Eastern Women

Skin - acne

Virilization - frontal balding, deepening of voice, increased muscle mass, clitoromegaly

269
Q

Excess androgen physical exam

A

body habitus

inspection: hair for balding and hirsutism (Ferriman-Gallwey score), skin acne, acanthuses nigricans, Cushingoid feature (moon face, buffalo hump, striae, thin skin, bruising), muscle mass

acanthosis nigricans = grey-brown discolouration of skin at neck, groin, axillae and vulva, which is marker of insulin resistance and hyper-insulinemia

abdominal exam: palpate for mass (ovary)

pelvic exam: inspect clitorus for clitoromegaly, bimanual pelvic exam for ovarian mass

270
Q

Excess androgen investigations

A

blood work for amenorrhea / oligo-menorrhea: b-hCG, prolactin, TSH, FSH

blood work for hirsutism: total and free serum testosterone, androstenedione, DHEA-S, 17-OH progesterone, dexamethasone suppression test or 24 hour urine for free cortisol

very high 17-OH progesterone (>200) in congenital adrenal hyperplasia

high cortisol despite dexamethasone suppression test or high 24 hour urine cortisol in Cushing’s syndrome

very high DHEA-S (>700) suggests androgen secreting adrenal tumor

high total testosterone (>150) suggest androgen secreting ovarian tumor

high androstenedione and high free & total testosterone suggest polycystic ovarian syndrome

if high total testosterone >150, trans-vaginal ultrasound for ovarian tumor

if high DHEA-S >700, abdominal CT with IV contrast for adrenal tumor

271
Q

Excess androgenism treatment

A

Oral Contraceptive Pill
indication: 1st line for treatment of acne and hirsutism
mechanism of action: estrogen increases steroid hormone binding globulin and progestin inhibits LH secretion, thereby decreasing ovarian androgen production
takes >6 months to be effective, usually stopped after 1-2 years and observe for return of ovulatory cycles

Spironolactone
indication: treats hirsutism
mechanism of action: inhibit ovarian and adrenal biosynthesis of androgen, androgen receptor antagonist, inhibit 5-alpha reductase activity
side effects: diuresis, theoretical risk of feminizing male fetus

Cyproterone Acetate
indication: treats acne and hirsutism
mechanism of action: inhibit androgen secretion, androgen receptor antagonist
side effect: fatigue, edema, loss of libido, weight gain, mastalgia

Dexamethasone
indication: congenital adrenal hyperplasia
mechanism of action: suppression of endogenous ACTH

Flutamide
mechanism of action: non-steroidal anti-androgen
side effect: hepatotoxicity

Finasteride
mechanism of action: inhibit 5-alpha reductase

Mechanical Methods
plucking, waxing, shaving or exfoliants, which do not destroy dermal papillae
electrolysis or laser, which destroy dermal papillae

272
Q

PCOS epidemiology

A

common endocrine problem in women of reproductive age

affects 5-10% of women of reproductive age (12-45)

273
Q

PCOS risk factors

A

Family history

metabolic syndrome (obesity, diabetes, dyslipidemia, hypertension)

274
Q

PCOS pathophysiology

A

insulin resistance -> decreased sex hormone binding globulin -> increased free testosterone
increased testosterone production by theca cells -> follicular atresia -> anovulation

anovulation results in no secretion of progesterone due to no corpus luteum, increased testosterone in ovary is converted to estrogen

thus high estrogen unopposed by progesterone lead to continuous endometrial proliferation that never shed, increasing risk of endometrial cancer

increased testosterone production and increased free testosterone -> secondary male sexual characteristics (hirsutism, virilization)

275
Q

PCOS signs and symptoms

A

onset usually around menarche, but can be after puberty

irregular menstruation or amenorrhea

infertility

acne, hirsutism, deepened voice

weight gain

vitals: hypertension
body habitus: overweight or obese
general: hirsutism, acne, male pattern baldness, acanthosis nigricans
pelvic exam: enlarged clitoris, large ovaries on palpation

276
Q

PCOS investigations

A

blood work: normal b-hCG, prolactin, TSH, FSH, normal to slightly high free & total testosterone <150, normal 17-OH progesterone, normal
dexamethasone suppression test, normal 24 hour urine cortisol test

high androstenedione

pelvic ultrasound: polycystic ovaries

277
Q

PCOS diagnosis

A

1) Exclude other causes for hyperadrogenism and amenorrhea
PCOS is diagnosis of exclusion

hyperandrogenism differential diagnoses

  • normal 17-OH progesterone ruling out congenital adrenal hyperplasia
  • normal 24 hour urine free cortisol ruling out Cushing’s syndrome
  • normal DHEA-S and normal abdomen ultrasound ruling out androgen secreting (adrenal or ovarian) tumor

amenorrhea differential diagnoses

  • negative b-hCG ruling out pregnancy
  • normal prolactin ruling out hyperprolactinemia
  • normal TSH ruling out thyroid disorder
  • no signs of structural abnormality besides polycystic ovaries on pelvic ultrasound
  • normal or low FSH ruling out primary ovarian insufficiency

2) diagnose PCOS based on Rotterdam’s criteria or AE-PCOS criteria

a) Rotterdam Criteria
patient diagnosed with PCOS if patient satisfies >2 of the 3 criteria
1. anovulation presenting as oligomenorrhea or amenorrhea
2. hyperandrogenism from clinical signs or high testosterone
3. polycystic ovaries (>12 cysts or large ovarian volume >10mL of at least one ovary) on ultrasound

b) Androgen Excess PCOS (AE-PCOS) Criteria
patient diagnosed with PCOS if patient satisfied all of the criteria below:
1. hyperandrogenism: hirsutism and / or hyperandrogenia
2. ovarian dysfunction: oligo or anovulation and / or polycystic ovaries on ultrasound
3. exclusion of other androgen excess disorders and related disorders

note that polycystic ovary on ultrasound is not enough to diagnose PCOS and patient without polycystic ovary on ultrasound can still have PCOS

278
Q

PCOS consequences

A 
1) Short Term Consequences
infertility
irregular menses
hirsutism, acne, androgenic alopecia
metabolic syndrome: insulin resistance, glucose intolerance, acanthosis nigricans, hypertension, obesity, dyslipidemia
obstructive sleep apnea
2) Long Term Consequences
PCOS increases risk of
type 2 diabetes mellitus
endometrial cancer
cardiovascular disease: coronary artery disease, myocardial infarction, stroke
279
Q

PCOS workup

A

work up need to assess for metabolic syndrome and cardiovascular disease risk

body habitus: BMI, waist circumference
blood pressure
diabetes screening: HbA1C and / or fasting blood glucose
lipid profile: total cholesterol, LDL, HDL, triglycerides

280
Q

PCOS treatment

A

1) Restore menorrhea
menorrhea restored by cyclic progesterone with withdrawal to stimulate cyclic shedding of endometrium
if patient does not want children, then combined oral contraceptive pill (OCP)
if contraception is not needed, then cyclic progesterone

2) Contraception
patients with PCOS can still get pregnancy, so need to use contraception if the patient does not want baby

3) Hyperandrogenism
OCP and Cyproterone acetate can be used to treat acne and hirsutism
Spironolactone can be used to treat hirsutism
hirsutism can be treated by mechanical means

281
Q

Management of PCOS complications

A

1) Metabolic Syndrome
regular assessment for metabolic syndrome including fasting glucose / HbA1C; lipid profile; blood pressure
healthy lifestyle: exercise, diet, weight loss
address each risk factor
antihypertensive if hypertensive
lipid lowering medication if hyperlipidemia
diabetes medication if diabetes mellitus
metformin can be used to treat impaired glucose tolerance

2) Endometrial Hyperplasia and Cancer
restore menorrhea by replacing progesterone to shed endometrium
endometrial biopsy to screen for endometrial cancer if age >35 and abnormal uterine bleeding

3) Infertility
contraception if patient does not want to get pregnant
ovulation induction with SERM (selective estrogen receptor modulator) as needed when patient want to get pregnant

282
Q

Infertility definition

A

failure to conceive after 1 year of frequent unprotected intercourse (frequent ~2-3 times during fertile time window, which is at ovulation around 14 days before menstruation)

283
Q

Infertility risk factors - female

A
  1. demographics: female age is single biggest risk factor for infertility, where chance of successful pregnancy dramatically decreases and miscarriage dramatically
    increases at age >35
    increasing age -> decreased follicle cells and lower quality of oocyte with higher risk of aneuploidy
  2. body habitus: very high or very low body mass index
  3. OB&GYN history: oligomenorrhea, amenorrhea, pelvic inflammatory disease, endometriosis
  4. past surgical history: previous abdominal or pelvic surgery
  5. medication: chemotherapy
284
Q

Risk factors for infertility - male

A
  1. demographics: age >40 years
  2. past medical history: history of undescended testes
  3. past surgical history: previous urogenital surgery
  4. medication: chemotherapy
  5. social history: recreational drugs
285
Q

Top 3 causes of infeertility not accounted for by female age

A
  1. Ovulation defect (oligomenorrhea or amenorrhea) in ~25% cases
  2. Male factor (ie abnormal semen quantity and/or quality) in 25% cases
  3. Fallopian tube defect in ~25% cases
286
Q

What is congenital bilateral absence of vas deference associated with

A

cystic fibrosis carrier

287
Q

Clinical evaulation for infertility is indicated for any of the following

A

couple in which female age <35 after 1 year of unprotected and frequent sexual intercourse

couple in which female age >35 or with specific medical history after 6 months of unprotected and frequent sexual intercourse

288
Q

Female causes of infertility

A
  1. Tubal factors- obstruction from surgery, inflammation, anatomical abnormality
  2. Ovulatory dysfunction - hypothyroidism, prolactinoma, hypothalamic amenorrhia, PCOS, POI
  3. Uterine structural abnormality - congenital uterine malformation, fibroids, adhesions, polyps
289
Q

Male causes of infertility

A
  1. Abnormal semen quantity and/or quality - lube, chronic disease, surgery, chemo, testosterone, smoking, alcohol, drugs, heat, Kleinfelter, CF, chromosome Y microdleetion
  2. Low or absent semen volume
    - failed emission, incomplete collection, short abstinence period, CBAVD, ejaculatory duct obstruction, hypogonadism, retrograde ejaculation
  3. Acidic semen -CBAVD, ejaculatory duct obstruction
  4. Azoospermia - obstruction, testicular failure
  5. Oligospermia - variocele, hypogonadism, T-chromosome microdelection
  6. Asthenospermia (poor sperm motility) - anti sperm antibodies, genital tract infection, partial obstruction of ejaculatory ducts, site of vasectomy reversal, varicele, prolonged abstinence
290
Q

Investigations of infertility

A

For all infertility all of the following assessment should be done:

  1. Assessment of ovulation by history and serum progesterone 7 days prior to expected period
  2. Ovarian reserve testing by FSH, estradial and pelvic ultrasound (us also assesses anatomy of uterus, uterine tube and rest of pelvis)
  3. Uterus and uterine tube anatomy on saline infusion sonogram or hysterosalpingogram
  4. Semen analysis
  5. TSH for thyroid dysfunction

investigation for oligo/anovulation only if positive history of olig/amenorrhea or low serum progesterone 7 days prior to expected period

291
Q

Assessment of ovulation

A

ovulation can be assessed by history, basal body temperature charting, urine LH detection kit or luteal phase progesterone
a) History
on history, a regular and predictable menstrual cycle lasting 21-35 days with signs of molimina (impending period) predict ovulation in 95% of women
signs of molimina include breast tenderness, cramping, mood changes and headaches
14 days before menstruation = ovulation
if patient has regular predictable period on history, then ovulation can be clearly predicted and no further investigation is required

b) Basal Body Temperature Testing
basal body temperature charting is tracking of basal body temperature throughout menstrual cycle with an accurate digital thermometer
increase of 0.3-0.5 C of body basal temperature correspond to 2-3 days after ovulation
having intercourse when basal body temperature have already increased is too late because it is 2-3 days after ovulation
charting of body basal temperature allows patient to track pattern of ovulation so that she can predict the next one given the same pattern

c) LH Surge
urine LH detection kit measures LH surge at ovulation, which can be used to detect current ovulation
having intercourse at LH surge as detected by LH detection is effective

d) Luteal Phase Serum Progesterone
progesterone need to be measured ~7 days before the expected menstrual period, which measure the elevated progesterone at the luteal phase if ovulation

292
Q

Investigations for oligo/anovulation

A

serum LH, FSH
serum estradiol (at day 3 of menstrual cycle)
serum progesterone (at 7 days before expected menstrual cycle)
serum b-hCG for pregnancy
serum TSH for thyroid function
serum prolactin for prolactinoma
pelvic ultrasound for any anatomical abnormalities

293
Q

Common causes of oligo/anovulation as determined by investigations

A

hypogonadotropic (low LH, FSH) hypogonadism (low estradiol, low progesterone) suggest central cause such as hypothalamic amenorrhea
normagonadotropic (normal LH, FSH) satisfying Rotterdam criteria (2/3 of polycystic ovaries on ultrasound, oligo / a-menorrhea and hyperandrogenism) suggest polycystic
ovarian syndrome
hypergonadotropic (high LH, FSH) hypogonadism (low estradiol, progesterone) suggest primary ovarian insufficiency
high TSH suggest hypothyroidism
high prolactin suggest prolactinoma

294
Q

Ovarian reserve definition

A

number of eggs remaining in ovary that have potential to ovulate and be fertilized

295
Q

How to count ovarian reserve

A

FSH and estradiol on day 3 of menstrual cycle

pelvic ultrasound which can count antral follicle as well as assess anatomy

low ovarian reserve if
high FSH and low estradiol and
low antral follicle count

ovarian reserve testing are not very reliable in predicting fertility potential

296
Q

How to confirm tubal patency

A

tubal patency assessed by hysterosalpingogram, saline infusion sonogram, or diagnostic laparoscopy

a) Hystersalpingogram (HSG)
HSG = injection of radio contrast dye into uterus and image on radiograph
normal patent uterine tube lead to contrast going from uterus to tube and into abdominal cavity, making uterus, uterine tube and some of the abdominal cavity visible on
radiograph
in tubal obstruction, the dye cannot enter uterine tube nor the abdominal cavity, so uterine tube and abdominal cavity is invisible
abnormal hysterosalpingogram leads to laparoscopic assessment
HSG best done in day 2-5 after menses (to avoid blood / clot, to ensure not pregnant) with NSAID and antibiotic (Doxycycline) prophylaxis (optional) prior to HSG due to 1-3% risk
of infection

b) Saline Infusion Sonogram (SIS)
SIS = infusion of saline into uterus, which can be visualized on ultrasound
SIS can be used as substitute for hysterosalpingogram
same principles and findings as hysterosalpingogram, where saline infusion in saline sonogram ~ contrast dye in hysterosalpingogram
SIS is better at assessing uterine cavity, but cannot assess tube structures
NSAID prior to SIS

c) Laparoscopy
laparoscopy is the gold standard test for assessing tubal factors
diagnostic laparoscopy is laparoscopic visualization of abdominal cavity while injecting dye (indigo carmine or methylene blue) into uterus
abnormal uterus / uterine tube anatomical abnormality can be visualized on laparoscopy such as fibrosis of uterus post pelvic inflammatory disease
normal patent uterine tube leads to dye going through uterine tube and exiting into abdominal cavity, which is visualized on laparoscope
obstructed uterine tube prevent dye from entering abdominal cavity, so it is not visualized on laparoscope
laparoscopy needs to be done under general anaesthesia, so it has operative risks
laparoscopic assessment indicated if patient has any of the below:
1. abnormal hysterosalpingogram
2. known endometriosis
3. previous ectopic pregnancy or tubal surgery
4. previous ruptured appendicitis
5. abnormal physical pelvic exam findings
6. previous pelvic inflammatory disease

297
Q

How to assess uterine factor for infertility

A

uterine factor is an uncommon cause of infertility

uterine factor usually already assessed by assessing for tubal patency and ovarian reserve with the following test:
1. pelvic ultrasound (3D ultrasound is better for assessing uterine malformation and space filling defects)

  1. HSG or SIS (can assess for space filling masses or intra-uterine adhesions)
  2. hysteroscopy, which is gold standard for definitive diagnosis of uterine abnormality
298
Q

Semen analysis

A

semen analysis is analysis of the male partner’s
semen sample which assess volume, concentration of sperm, sperm motility and sperm morphology

semen analysis should be at least 2 properly performed semen analysis obtained at least 4 weeks apart with abstinence 2-3 days prior to semen collection, which are transported at
body temperature and analyzed within an hour

normal semen analysis according to WHO criteria is:

  1. volume >1.5mL
  2. pH >7.2
  3. sperm concentration >15 million/mL of semen
  4. sperm motility >40% progressive
  5. sperm morphology >4% normal
299
Q

Hypospermia definition

A

small semen volume

300
Q

oligospermia definition

A

low sperm count

301
Q

azoospermia definition

A

absence of sperm in semen

302
Q

asthenozoospermia definition

A

low sperm motility

303
Q

teratospermia definition

A

sperm with abnormal morphology

304
Q

oligoasthenoteratozoospermia definition

A

low sperm count with low motility and abnormal morphology

305
Q

Hypogonadotropic (low LH, FSH) hypogonadism (low estradiol, low progesterone) such as hypothalamic amenorrhea treatment

A

weight gain

GnRH pump or gonadotropin (FSH) SC infection to induce ovulation

In-vitro fertilization

306
Q

Normagonadotropic (normal LH, FSH) normoestrogenic such as polycystic ovarian syndrome (PCOS) treatment

A

Weight loss

1st line - Clomiphene citrate (SERM acting as estrogen antagonist thereby increasing FSH) to induce ovulation

Aromatase inhibtor

insulin sensitizing agent (Metformin)

Laparoscopic ovarian drilling to induce ovulation

Gonadotropin (FSH) SC injection to induce ovulation

In-vitro fertilization

307
Q

hypergonadotropic (high LH, FSH) hypogonadism (low estradiol, progesterone) such as primary ovarian insufficiency treatment

A

in-vitro fertilization

donor egg

adoption

308
Q

treatment of tubal factor infertility

A

consider tubal surgery

in-vitro fertilization

309
Q

treatment of uterine factor infertility

A

surgical removal of masses or adhesions within uterine cavity

310
Q

treatment of male factor infertility

A

lifestyle modification: avoid excessive heat, limit caffeine intake, stop smoking, stop marijuana and other recreational drugs, decrease alcohol intake, vitamins (C, E, Selenium, Zinc,
Folic acid)
abnormal sperm production: gonadotropin or exogenous pulsatile GnRH for hypothalamic dysfunction
abnormal sperm function: intra-uterine insemination, in-vitro fertilization
obstruction: in-vitro fertilization with testicular sperm aspiration / extraction (TESA / TESE)

311
Q

Treatment modalities of infertility in order of increasing success rate and invasiveness

A

Ovulation induction –> OI with IUI –> superovulation with IUI –> IVF

312
Q

Ovulation induction definition, indications, contraindications and method

A

ovulation induction = supra-ovulation = inducing ovulation of 1 egg

ovulation induction / supra ovulation stimulate ovulation followed by sexual intercourse with partner to improve chance of pregnancy

ovulation induction / supra-ovulation indicated in oligo / an-ovulation

ovulation / supra-ovulation should not be used in

  1. premature ovarian insufficiency
  2. regular menstruation and ovulation where ovulation is not the cause for infertility
  3. mild male factor as cause of infertility
  4. unexplained infertility

ovulation / supra ovulation can be induced by clomiphen citrate, tamoxifen, letrazole, gonadotropin (FSH) or ovarian drilling

313
Q

Clomiphene citrate mechanism

A

selective estrogen receptor modulator (SERM) that acts as an estrogen antagonist at the hypothalamus
estrogen antagonism at hypothalamus remove negative feedback of estrogen, increasing FSH
increased FSH stimulate follicular development and thus stimulate ovulation

314
Q

Tamoxifen MOA

A

SERM that block estrogen effect on hypothalamus to increase FSH and stimulate follicular development & ovulation

315
Q

Letrazole MOA

A

aromatase inhibitor that decrease synthesis of estrogen level, stimulating FSH release and triggering follicular development & ovulation

316
Q

Gonadotropin (FSH) administration for infertility

A

given as a daily subcutaneous injection in follicular phase with ultrasound monitoring of developing follicles to trigger ovulation

317
Q

SERM risk

A

repetitive cycles of SERM >12 increase risk of ovarian and breast cancer

318
Q

Ovarian drilling method for infertility

A

surgical caudery of tiny holes in stroma of ovary, decreasing androgen release from theca cells, stimulating ovulation

ovarian drilling associated with risk of bleeding and tubal obstruction

319
Q

Superovulation definition, indication, method

A

superovulation = inducing ovulation of 2-4 eggs

superovulation artificially induce ovulation followed by usually intrauterine insemination

superovulation is a more extreme version of ovulation induction, so it is usually used in combination with intrauterine insemination when ovulation induction with intrauterine
insemination fails

superovulation is done with daily subcutaneous FSH injection under concomitant ultrasound to track follicular development (high FSH dose induce maturation and ovulation of >1 egg)

320
Q

What’s the deal with IUI (pairing, method, benefit)

A

IUI usually paired with OI or SO to increase chance of conception

in IUI, sperm sample is taken from the male partner, which is then washed to filter and keep only the viable and mobile sperm

the washed sperm sample is then inserted via an insemination catheter into the uterus at same time as OI or SO

IUI is better than natural sexual intercourse at conception because it is an optimal placement of washed sperm

321
Q

OI with IUI indications and disadvantages

A

indicated in
unexplained infertility
oligo / ano-ovolation where OI alone failed
moderately low sperm counts

disadvantages include
time consuming with frequent visits, tests and procedures
emotionally demanding
expensive
risk of multiple pregnancy and ovarian hyperstimulation

322
Q

SO with IUI indications and disadvantages and success rates

A

indicated in
cases where OI with IUI failed

same disadvantages as OI with IUI

success rates are moderate
20% success rate in women age <35
10-15% success rate in women aged 35-39
<10% success rate in women aged 40

note that success rate of SO with IUI is greater than OI with IUI

323
Q

IVF definition, indication, procedure, success rates

A

in vitro fertilization is stimulation of follicle which is then retrieved and fertilized with sperm in-vitro followed by re-insertion of fertilized embryo back into uterus to be implanted

indication for in-vitro fertilization

  1. tubal obstruction
  2. severe endometriosis
  3. severe oligo-azoospermia (very low sperm count)
  4. polycystic ovarian syndrome with failed medical therapy
  5. failed SO with IUI at least 3 times
  6. donor egg is needed (e.g. primary ovarian insufficiency)
  7. advancing maternal age (>40)

general procedure have 4 steps
1) FSH stimulation by subcutaneous injection to grow multiple follicles under close ultrasound and bloodwork monitoring
2) egg is aspirated with needle inserted through vagina into ovary under ultrasound guidance
3) retrieved egg is fertilized with sperm to make embryo by standard in-vitro fertilization or intra-cytoplasmic sperm injection (ICSI)
a) in standard in-vitro fertilization, egg is mixed with solution of millions of sperm and one of those sperm will fertilize the egg, resulting in embryo
b) in ICSI, 1 sperm is chosen and then inserted into the egg resulting in embryo
c) standard in-vitro fertilization or ICSI depend on sperm count, motility and morphology where ICSI preferred if male partner sperm sample have low count, low motility and low
percentage of normal morphology
d) the fertilized embryo will be grown in petri-dish for 3-5 days (emulating days embryos traverse through uterine tube before implantation)
e) good quality fertilized embryos can be frozen (cryoperserved) for future use
4) fertilized embryo is then inserted via catheter into uterus under ultrasound guidance, so that it can implant into uterus and start pregnancy
a) in young women (<38), 1 or 2 fertilized embryos is inserted into uterus hoping 1 will implant
b) in older women (>42), 5 fertilized embryos is inserted into uterus hoping 1 will implant

IVF have highest success rate
overall success rate ~40% in all women
~50% success rate in women age <35
~40% success rate in women age 35-39
~20% success rate in women age >40
324
Q

Time limit for collecting forensic evidence and using rape kit in suspected domestic violence case

A

72h

325
Q

When is STD prophylaxis administered in suspected domestic violence cases

A

Within 72h of potential exposure (contact with perpetrator’s genitalia)

326
Q

Gonorrhea prophylaxis

A

Ceftriaxone 250 mg IM 1 dose

or Cefixime 400 mg PO 1 dose

327
Q

Chlamydia prophylaxis

A

Azithromycin 1g PO 1 dose

or Doxycycline 100 mg PO q12h for 7 days

328
Q

Trichomoniasis and BV prophylaxis

A

Metronidazole 2g PO 1 dose

329
Q

Hep B prophylaxis

A

hep b vaccine if unvaccinated (asap, then repeat doses at 1-2 months and 4-6 months after 1st dose)

330
Q

HIV

A

Zidovudine (AZT) 200mg PO Q8H or 106mg/m2 per dose Q8H for 4 weeks PLUS Lamivudine 150mg per dose Q12H or 4mg/kg per dose Q12H for 4 weeks
consider HIV prophylaxis if assailant is known to be HIV positive or is at high risk for being HIV positive
alternative for adolescents: 300mg AZT / 150mg Lamivudine Q12H for 4 weeks

331
Q

Emergency contraception

A

Levonorgestrel 0.75 mg once then repeated in 12h

332
Q

Components of the pelvic floor

A 
Peritoneum 
Pelvic viscera 
Endopelvic fascia 
Elevator ani muscle 
Perineal membrane 
Superficial genital muscles 
Vulvar subcutaneous fascia 
Fat 
Skin
333
Q

What is the genital hiatus

A

Oval opening between the levator crura through which passes the vagina and urethra

334
Q

How does the vaginal uterine axis change with position

A

vaginal uterine axis is parallel to long axis of body when supine, but when standing, lower 1/3 vagina is parallel to the long axis of body but the upper 2/3 vagina & uterus are
perpendicular to long axis of body

335
Q

Support of vagina and uterus

A

Structural Support
anterior support: lower 1/3 vagina supported by pubouretral and urethropelvic ligament, which contains elastin and collagen with smooth muscle
lateral support: lower 1/3 vagina supported by endopelvic fascia which attaches to the arcus tendineus; upper 2/3 vagina & uterus supported by cardinal (Mackenrodt’s) ligament
posterior support: uterus supported by uterosacral ligament
apical support: uterosacral ligament and upper support of arcus tendons

2) Mechanical Support
constant levator ani muscles contraction activity pulls rectum anteriorly & superiorly, help maintain urinary & fecal incontinence
(levator ani muscle involuntarily contracts during cough)
cardinal and uterosacral ligaments, pubo-cervical fascia
flap valve closure: upper vagina covers opening in levator plate

once one of the supports fails, then progressive damage to other supports over time due to extra strain, leading to pelvic organ prolapse

336
Q

Overactive bladder definition

A

syndrome of urgency, frequency, nocturia, urinary incontinence

337
Q

Risk factors for all urinary incontinence

A

Immobility

338
Q

Risk factors for stress incontinence

A

Chronic valsalva maneuvers

Pelvic floor relaxation

Pregnancy and childbirth

339
Q

Risk factors for urgency incontinence

A

Medication

Smoking

Obesity

340
Q

Risk factors for overflow incontinence

A

Neurologic problems

Medication

341
Q

Etiology of urgency incontinence

A

a) detrusor overactivity
- neurologic (spinal cord injury)
- inflammation (cystitis, stone, tumour)
- structural (bladder neck obstruction tumour stone, BPH)
- idiopathic

b) decreased bladder compliance
- fibrosis of bladder
- non-functioning bladder neck or proximal urethra: neurological disease, trauma, surgery, aging

342
Q

Stress incontinence etiology

A

a) Urethral hypermobility
- childbirth
- pelvic surgery
- aging
- levator muscle weakness

b) intrinsic sphincter deficiency
- aging
- hypoestrogen state
- pelvic surgery
- neurologic problem

343
Q

Urethral hypermobility definition

A

weakened pelvic floor allowing bladder neck and urethra to descend with increased intra abdominal pressure

344
Q

Overflow incontinence clinical presentation

A

Supra-pubic pressure

Over distended bladder

Continuous incontinence

345
Q

What medications can contribute to urinary incontinence

A 
anti-histamine
anticholinergics
ACE inhibitor, diuretics
anti-depressants, antipsychotics
alpha agonists, alpha 1 blockers
346
Q

What is the q tip test

A

for urinary incontinence

insert cotton swab into urethra, where positive test = movement of swab by >30 degrees with straining which suggest urethra hyper mobility causing stress urinary
incontinence

347
Q

What is a bulbocavernosal reflex and what levels does it test

A

(S2-4): anal sphincter contraction with squeezing of clitoris, bulb penis or tugging of Foley catheter

348
Q

What is an anal wink and what levels does it test

A

(S2-4): ipsilateral contraction of anal sphincter upon stroking of the peri-anal skin

349
Q

Investigations with urinary incontinence

A

Urine analysis R&M, C&S

Suspected overflow - post void residual u/s

suspected urgency - cystometry to diagnose detrusor overactivity

severe voiding symptoms - urine flow rate and urodynamic testing

suspected structural disease within urethra or bladder - cystoscopy

350
Q

Urgency incontinence diagnosis

A

Based on history and urodynamics study

351
Q

Stress incontinence diagnosis

A

History and positive stress test on physical

352
Q

Overflow incontinence diagnosis

A

bladder u/s showing PVR > 200 cc

353
Q

Stress incontinence management

A

1st line = lifestyle modification, weight loss, pelvic floor exercises (Kegel, vaginal cones, biofeedback, electrical stimulation), bulking agents, estrogen replacement therapy
2nd line = pessary for female (medical device to provide structural support of vagina)
last line = surgical treatments
open or laparoscopic Burch Retropubic Urethropexy (RPU), where placing surgical suture at bladder neck and tying it to Cooper ligament
pubo-vaginal sling procedures, where a band of sling is placed under bladder neck that tightens (closing urethra) during Valsalva maneuver
mid-urethral slings, which can be retropubic tension-free vaginal tape (TVT) or obturator TVT, where a sling is placed around mid urethra that tightens (closing urethra) during
Valsalva maneuver
surgical treatments have 80-90% cure rate at 5 years

354
Q

Urgency incontinence

A

1st line = lifestyle modification (decrease fluid intake, limit caffeine intake, smoking cessation, weight loss), bladder habit training, estrogen replacement therapy
2nd line = medication: anti-cholinergics (Tolterodine, Oxybutynin, Trospium, Solifenacin, Darifenacin, TCA)
last line = Botulinum toxin, sacral neuromodulation
no role for surgery

355
Q

Mixed incontinence management

A

combination of management for urgency and stress incontinence

356
Q

Overflow incontinence management

A

lifestyle changes
catheterization
treat underlying cause

357
Q

Pelvic organ prolapse definition

A

herniation of pelvic organs to or beyond the vaginal walls

358
Q

anterior compartment prolapse definition

A

herniation of anterior vaginal wall often associated with descent of bladder (cystocele) and urethra (urethrocele)

359
Q

posterior compartment prolapse definition

A

herniation of posterior vaginal wall often associated with descent of rectum (rectocele) and / or intestines (enterocoele)

360
Q

apical compartment prolapse definition

A

descent of apex of vagina (uterus and cervix, cervix alone or vaginal vault) into lower vagina to hymen or beyond vaginal introitus, can be associated
with enterocele

361
Q

uterine procidentia

A

anterior, posterior and apical compartment prolapse

362
Q

Pelvic organ prolapse risk factors

A

demographics: age
OB&GYN history: pregnancy, vaginal childbirth (which stretches pelvic muscle and fascia that may cause permanent damage)
body habitus: obesity
past medical history: previous pelvic surgery
other: hypo-estrogenic state (post-menopause), connective tissue disorder
social history: smoking

363
Q

Pelvic organ prolapse pathophysiology

A 
contributing factors lead to weakness in pelvic floor that hold pelvic organs in place including
aging
declining quality of collagen
estrogen withdrawal
constipation
chronic cough

weakness in pelvic floor structures lead to prolapse of organs herniating into vaginal wall, which descends into what was originally vaginal canal

364
Q

Pelvic organ prolapse clinical presentation

A

sensation of fullness, pressure or bulge in vagina
organs falling out of vagina
urinary symptoms: urinary incontinence or retention (may be complicated by urinary tract infection or renal impairment)
– pelvic organ prolapse may mask stress urinary incontinence by organ compressing on urethra, which is important, because any surgery fixing pelvic organ prolapse will create
new problem of stress incontinence
GI symptoms: constipation
OB&GYN symptoms: vaginal bleeding or discharge from erosions or ulcerations

365
Q

Stages of pelvic floor prolapse

A

grade 0 = no prolapse
grade 1 = prolapse descending to upper 1/3 of vagina
grade 2 = prolapse descending to mid vagina
grade 3 = prolapse descending to level of hymenal ring or introitus
grade 4 = prolapse descending past hymenal ring

366
Q

Pelvic organ prolapse management

A

treatment is indicated for any symptomatic pelvic organ prolapse
1st line = pelvic floor exercises (Kegels, vaginal cones, biofeedback, electrical stimulation of pelvic floor), estrogen replacement therapy (systemic or local)
2nd line = pessary (medical device inserted into vaginal canal to provide structural support to return and hold prolapsed organ to its original place)
last line = surgery

367
Q

Absolute indication for surgery in pelvic organ prolapse

A

urinary retention due to organ prolapse (which may lead to hydronephrosis and renal failure), otherwise all other surgeries are elective procedures

368
Q

At what stage is surgery considered for pelvic organ prolapse

A

Stage 3-4

369
Q

What are the options for surgery for pelvic organ prolapse

A

surgery can be reconstructive or obliterative
reconstructive aims to correct and restore normal anatomy, which can be via open or vaginal approach
in reconstructive surgery, supporting structures (uterosacral ligament, sacrospinous ligament) are reattached or shortened; or organs are pexed (tethered) to other internal
pelvic structures to prevent prolapse via mesh
vault prolapse: sacralcolpopexy, sacrospinous fixation, uterosacral ligament suspension
cystocele: anterior colporrhaphy (plication of pubovervical fascia), may use graft to provide support which can be sutured to cardinal uterosacral ligament, endopelvic
fascia or obturator fascia
rectocele: posterior colporrhaphy (posterior repair), plication of endopelvic fascia and perineal muscle approximated in midline to support rectum and perineum
enterocele: contents reduced, neck of peritoneal sac ligated, uterosacral ligament and levator ani muscle approximated

obliterative removes and / or closes off all or portion of vaginal canal by colpocleisis (closure of vagina) or colectomy to reduce viscera back into pelvis, which is only via
vaginal approach

370
Q

Potential complications of pelvic organ prolapse surgery

A

urinary incontinence, dyspareunia, recurrence of relapse (30% risk)

371
Q

Fistula etiologies

A

Obstetric

Iatrogenic

Local disease causing inflammation

372
Q

Pathophysiology of obstetric fistula

A

obstetric fistula usually result from prolonged, obstructed labour without timely medical intervention

1) prolonged, obstructed labour result in sustained pressure of baby’s head on mother’s pelvic bone, damaging pelvic soft tissue
2) damage of pelvic soft tissue result in fistula from vagina to bladder or rectum

373
Q

Gynecological fistula clinical presentation

A

vesicovaginal or rectovaginal fistula: recurrent vaginitis, irritation of vulva, vagina and perineum, dyspareunia

vesicovaginal fistula: uncontrolled leakage of urine into vagina (“urinary incontinence” or “increased vaginal discharge” by patient), recurrent urinary tract infection, abnormal urinary
stream, hematuria

rectovaginal fistula: uncontrolled leakage of feces into vagina (“fecal incontinence” or “foul smelling vaginal discharge” by patient), flatus into vagina

374
Q

Gynecological fistula management

A

A) Vesicovaginal fistula
if small fistula, then trans-urethral or supra-pubic catheter to drain bladder, allowing fistula to heal
if large fistula, then surgical repair (lysis of fistula and then closure of fistula with sutures), which can be via vaginal or abdominal open approach
B) Rectovaginal fistula
surgical repair (lysis of fistula and then closure of fistula with sutures), which can be via vaginal or abdominal open approach

375
Q

Menopause definition

A

last natural menstrual period, defined as 12 months of amenorrhea after the last natural menstrual period, typically occurring at age 45-55

376
Q

Early menopause time frame

A

40-45 years

377
Q

Primary ovarian insufficiency / premature ovarian failure time frame

A

menopause before age 40

378
Q

Late menopause time frame

A

after 55 years

379
Q

peri- menopause definition

A

transition period of altered ovarian hormone leading up to menopause and 1 year after menopause

380
Q

Peri-menopause time frame

A

progression from regular cycles to shortened cycles to irregular cycles then to menopause
peri-menopause can start as early as mid 30s and last 2-8 years up to menopause

381
Q

average age of menopause

A

51 years

382
Q

Physiology of menopause

A

in time around menopause, there is narrowing of thermoneutral zone, which result in regulatory response of sweating or shivering in response to small change in temperature

loss of estrogen lead to atrophy of vagina and bladder incontinence

low estrogen lead to dyslipidemia, increase plaque development and inhibit vasodilation, thereby increasing risk of cardiovascular disease

383
Q

Menopause clinical presentation

A

symptoms can be throughout peri-menopause and post-menopause
there is spectrum of symptoms, where menopause can range from asymptomatic to symptomatic severely affecting quality of life
Symptoms
vasomotor: hot flashes, night sweats
affect ~60% of menopausal women
majority of post-menopausal women will experience hot flashes <7 years, but hot flashes can persist for >15 years
exacerbated by obesity, smoking
usually have trigger such as alcohol, warm ambient environment, hot drinks
cognitive: poor memory, poor concentration
psychiatric: depression, irritability, emotional lability, sleep disturbance
menopause can initiate de novo psychiatric disorder or worsen existing psychiatric disorder
urogenital: vaginal dryness, urinary frequency & urgency, diminished libido
vaginal dryness often 1st sign of menopause and progressive with time, leading to discomfort, dyspareunia, bleeding, post-coital bleeding or discharge
general: fatigue, myalgia & athralgia
complication due to low estrogen in post-menopause: increased risk of cardiovascular disease, osteoporosis, colorectal cancer

384
Q

Contraindication for hormonal therapy in menopause

A

hormone dependent cancer: breast cancer, endometrial cancer
arterial thromboembolic disease: myocardial infarction, angina
venous thromboembolism: deep vein thrombosis, pulmonary embolism
cardiovascular disease: coronary artery disease, myocardial infarction, stroke
severe active liver disease
un-investigated abnormal uterine bleeding due to possible endometrial cancer and hormone replacement worsening uterine bleeding

385
Q

Hormonal profile in menopause

A

FSH, LH, and E2 tend to fluctuate during menopause and usually not used, also due to the fact that peri-menopause and menopause are clinical diagnoses
usually menopause have high FSH, high LH and low E2

386
Q

Investigations in menopause

A

cardiovascular disease risk factors: lipid profile, blood glucose / HbA1C
cancer risk factor: mammogram
osteoporosis risk factor: BMD
pelvic ultrasound as baseline, which can be used to compare and detect endometrial hyperplasia post hormone replacement

387
Q

diagnosis of menopause

A

clinical retrospective diagnosis which rarely requires investigation - diagnosed if amenorrhea for 1 year and in normal age range (45-55)

388
Q

Management of menopausal symptoms

A

lifestyle modification recommended for everyone
reducing core body temperature (fan, reduce room temperature, lighter clothing)
regular exercise
weight loss
smoking cessation
avoid known trigger such as hot drinks or alcohol
for vasomotor symptoms, consider prescribing systemic hormonal therapy (HT)
45
for urogenital atrophy, prescribe local vaginal estrogen

389
Q

What is the systemic hormonal therapy used in menopause

A

Estrogen and progesterone if patient has an uterus OR estrogen only if patient does not have an uterus

390
Q

Systmeic hormonal therapy vs oral contraceptive pill

A

HT is not equivalent to OCP
HT is at a lower dose which only partially replaces the estrogen and progesterone hormone level to a level below normal whereas OCP is at a higher dose which increases estrogen
and progesterone hormone to a level above normal
HT is safer than OCP due to lower doses
contraindication for HT and OCP are not the same

391
Q

HT indication

A

indication: menopausal symptoms (vasomotor, vaginal dryness) that is negatively impacting quality of life to be started in critical window (3-5 years after last menstrual
period) for maximum of 5 years therapy

in patients with premature ovarian failure, HT should be used up until normal menopause age (i.e. age 50) for its cardio-protective effect

HT is not recommended for prevention of coronary heart disease or osteoporosis due to risk of breast malignancy and cardiovascular disease

392
Q

HT contraindication

A

cardiovascular disease: stroke, coronary artery disease, myocardial infarction
VTE related: smoking, previous VTE including DVT, PE
malignancy: previous breast cancer, endometrial cancer
acute liver disease

393
Q

HT mechanism in menopause

A

hormonal therapy replaces low estrogen in menopause, negating menopausal symptoms as well as negating health risks associated with low estrogen
progesterone is added to lower risk of endometrial cancer from unopposed estrogen
estrogen only HT can be considered in patients with total hysterectomy

394
Q

Types of HT

A

types of estrogen
oral conjugated equine estrogen (CEE/premarin), which is not bio-identical
oral estrase, which is bio-identical
transdermal estradiol, which is bioidentical

types of progesterone
oral micronized progesterone, which is bio-identical
progestin, which is a synthetic drug and not bio-identical

395
Q

HT routes of administration

A

estrogen can be delivered orally or transdermally (gel, patch)
oral estrogen is inferior to transdermal, because it increases risk of VTE
the transdermal patch bypass liver to avoid VTE risk, are relatively stable in blood and permit measurement of serum estradiol for dose adjustment
transdermal estrogen route includes gel and patch
progesterone is usually delivered orally

396
Q

HT and CVD risk

A

no convincing evidence that HT increase risk of CVD in newly menopausal women starting HT
HT started in critical window (3-5 years after last menstrual period) do not increase CVD risk
HT initiated outside critical window (>5 years after last menstrual period) can increase CVD risk

397
Q

HT and VTE risks

A

HT only increase VTE risk by a minimal amount (2-3 additional cases per 10,000 users) with greatest risk in 1st year of use
risk of VTE decreases with lower dose and transdermal route of estrogen

398
Q

HT and Stroke and dementia risks

A

HT as risk for stroke and dementia is unclear
risk factors for stroke should be addressed
HT should be on the lowest dose

399
Q

HT and breast cancer risk

A

longer duration of HT increases risk of breast cancer (8 additional cases per 10,000 person years)
usually breast cancer risk increases after 5 years of HT
patients taking HT should undergo regular screening for breast cancer

400
Q

HT General usage guidelines during menopause

A

start HT with a low dose and then slightly increase until menopausal symptoms improve thus to be at minimally effective dose
while on HT, reassess risk for CVD, VTE and breast cancer regularly
stop HT by age of 60 or after 5 years of HT due to increased risk for CVD and breast cancer
if possible, use transdermal estradiol to decrease risk of VTE
if patient have uterus, add micronized progesterone

401
Q

HT side effects

A

mood symptoms
breast soreness
bloating
vaginal bleeding

402
Q

alternative therapies to HT

A

if hormonal therapy is contraindicated or not desired, then 2nd line treatments may be considered for vasomotor symptoms
anti-depressant: venlafaxine (Effexor), desvenlafaxin
anti-epileptics: gabapentin
anti-hypertensives: clonidine
venlafaxine and gabapentin are most commonly used
complementary and alternative therapy is not recommended due to lack of evidence for efficacy and safety

403
Q

Local vaginal estorgen indication

A

1st line treatment for vaginal atrophy in absence of vasomotor symptoms
can be added to HT if HT does not resolve vaginal atrophy

404
Q

Types of local vaginal estrogen

A

cream: premarin vaginal cream, estragyn cream
vaginal suppository: vagifem
vaginal ring: estring

405
Q

Local vaginal estrogen risks

A

Due to only local effect, local vaginal estrogen not associated with CVD, VTE nor breast cancer

406
Q

Local vaginal estrogen general guidelines

A

local vaginal estrogen need to be taken life-long

3rd year - Obstetrics and Gynecology (7 decks)

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