GOSH Flashcards
What is a speculum examination
Insertion of a speculum device to facilitate the inspection of the vaginal wall and ectocervix
Evaluation of the quality of vaginal discharge to determine whether a smear should be acquired
What is the ectocervix and what type of cells make it up
Outer part of the cervix, distal to the uterine external os
The mucosal surface of the vaginal cervix.
Lined with nonkeratinized stratified squamous epithelium.
What are the signs and symptoms of pathologic discharge
Malodorous Abnormal consistence (frothy or curd like) Bloody, brown, yellow, green or gray colour
Puritic and/or erythematous vagina
Cervical tenderness
What is physiological leukorrhea
Profuse white or yellow and non-malodorous vaginal discharge can be physiological if none of the other symptoms of pathologic discharge are present
In newborns, vaginal discharge may occur due to in-utero exposure to maternal oestrogen (no treatment necessary)
What is Important about speculum exams in preadolescent patients
Nearly never indicated but if absolutely necessary (eg vaginal bleeding, trauma or abuse) it is usually done under general anaesthesia
What is a colposcope
A type of microscope used to acquire a magnified view (6-40x) of the vaginal wall or ectocervix
Can detect pracancerous and cancerous lesions with application of acetic acid or iodine
Can be used for colposcopy directed cervical smears and biopsies
Can be used in surgical procedures
What is cervical ectopy
A state in which the squamous cell epithelium of the ectocervix is replaced by columnar cell epithelium of the endocervix under the physiological influence of oestrogen (eg precnancy, certain oral contraceptives)
Can be seen on colposcopy as a sharply demarcated bright red area with papillary structures
Clinical features: mostly asymptomatic, occasional postcoital bleeding and vaginal discharge
Predisposition to chlamydial infection
Malignant transformation may occur in cases of HPV-16 and/ or HPV-18 infections
What is the transformational zone
The area between the non-keratinised squamous epithelium of the ectocervix and the columnar epithelium of the endocervix.
It is a common site for infections and dysplastic changes
What are nabothian cysts
Retention cysts that arise in the transformational zone
These have no pathological significance
What are cervical polyps
Hyperplastic cervical epithelium
Clinical features: vaginal bleeding
Malignant degeneration is rare
Treatment: surgical resection of the polyp and cauterization of the polyp’s pedicle to prevent recurrence
What are the abnormal findings on colposcopy
All require further evaluation
Condylomata acuminata: white lesions under acetic acid application
Cervical leukoplakia: white membrane that cannot be scraped off
Cervical intraepithelial neoplasia: punctate lesions or coarse mosaic pattern
Cervical cancer: atypical vessels
What is the normal finding on a vaginal smear
Cylindrical Lactobacilli (Doderlein’s bacilli)
What are the pathological findings on a vaginal smear and what is the subsequent diagnosis
Pseudomycelia and/or yeast cells: Vaginal candidiasis
Motile flagellated protozoa: Trichomoniasis
Clue cells and positive whiff test: Bacterial vaginosis
Estimate pH levels:
- Normal 4 - 4.5
- > 4.5 then suspect bacterial infections (other causes could be menstruation, amniotic fluid and sexual intercourse)
Also need to do bacterial culture and sensitivity analysis if bacterial infections due to an unknown pathogen are suspected
PCR and/or serological tests can be done for suspected chlamydial infections or HPV typing
What is involved in a Whiff test
AKA: Amine test, Hinsberg reaction
Positive if adding 1–2 drops of 10% KOH (potassium hydroxide) to vaginal fluid (on the speculum after the pelvic examination/on a microscope slide) leads to an intensification of the fishy odor.
What is the tumour marker for breast carcinoma
CA 15-3
What is the tumour marker for ovarian and/or endometrial carcinoma
CA 125
What is the tumour marker for squamous cell carcinoma (eg cervical, vulval and/ or vaginal carcinomas)
SCC
What is the tumour marker for germ cell tumours
AFP
What is the tumour marker for choriocarcinomas and or/ germ cell tumours
HCG
What is a transabdominal ultrasound used for
The easiest menthof of assessing the uterus, ovaries and adnecal structures
Used in assessment of:
- Urogenital tract
- Foetal development
- Pelvic organs
What is a transvaginal ultrasound used for
Performed to diagnose ovarian cysts, tumors and follicular maturation
Looking at uterus:
- Myometrium (eg to diagnose leiomyomas)
- Endometrium:
- echogenic layer in the long axis view of the uterus (endometrial stripe)
- endometial thickness varies with menstrual cycle
- postmenopausal women with an endometial thickness >8mm should undergo a follow up ultrasound 1-3 months later
- postmenopausal women with an endometrial thickness >10mm should undergo hysteroscopy and endometrial curettage to rule out endometrial carcinoma
Assessment of foetal development during first trimester
Meausrement of cervical length in cases of cervical incompetence
What is breast ultrasound used for
Used to assess breast lesions which were detected by palpation, mammography, and/or breast MRI scans
Can also be used to assess the axilla for lymph node involvement if there is suspicion for breast cancer
What is hysteroscopy
A fiberoptic scope is introduced transcervically into the uterus to diagnose and/or treat uterine pathologies
Commonly done as part of the work up of abnormal uterine bleeding
Can be combined with diagnostic/ therapeutic uterine curettage
What is uterine curettage
Scraping away endometrial tissue by introducing a curette into the uterine cavity
What are the Müllerian ducts
A pair of embryonal ducts that give rise to the fallopian tubes, uterus, cervix, and upper one-third of the vagina in a female foetus.
In a male fetus, the production of Müllerian inhibiting factor by the Sertoli cells of the testes causes degeneration of the Müllerian (or paramesonephric) ducts.
What are the anomalies of Müllerian duct fusion
Incidence: 3-4/100 females
Pathophysiology:
- defective fusion of the Müllerian ducts during embryonal development
- normally functioning gonads and female karyotype results in normal development of secondary sexual characteristics (eg breast, pubic hair development)
What are the types of Müllerian duct fusion anomalies
Müllerian agenesis: Both of the Müllerian ducts fail to develop, leading to the absent or hypoplastic uterus, absent cervix, and vaginal agenesis (but functional ovaries)
Unicornuate uterus: One of the Mullerian ducts fails to develop
Didelphic uterus: Complete lack of Mullerian duct fusion resulting in double uterus, double cervix, double vagina
Bicornuate uterus: Incomplete fusion of the mullerian ducts to various degrees:
- Uterus bicornis unicollis - double uterus, single cervix, and single vagina
- Uterus bicornis bicollis - double uterus and double cervix with/without a vaginal septum
Septate uterus: The mullerian ducts fuse, but the septa between the two ducts persists either partially (subseptate uterus) or completely (septate uterus)
DES-related abnormality: In utero exposure to diethylstilbestrol:
- Vagina: adenosine, adenocarcinoma
- Cervix: cockscomb cervix, cervical collar
- Uterus: hypoplasia, uterine synechiae, T shaped uterine cavity
- Fallopian tube: abnormal fimbriae, cornual budding
What are the clinical features of Mullerian duct fusion anomalies
Asymptomatic before puberty
Infertility and dyspareunia
In some cases, periodic lower abdominal pain
Menorrhagia
Amenorrhea
Associated urological (25-50% of cases) and skeletal (10-15% of cases) malformations
Increased risk of these obstetric complications:
- ectopic pregnancy
- cervical incompetence
- preterm labor
- malpresentation
- obstructed or prolonged labour
-retained placenta leading to postpartum haemorrhage
What is dyspareunia
A symptom of pain that occurs during or after sexual intercourse.
What is menorrhagia
A condition of abnormally high flow of bleeding (> 80 mL of bleeding volume) or prolonged duration of bleeding (> 8 days of menstruation) during menstrual periods.
What is malpresentation
An obstetric term that refers to a foetus with a part other than the head overlying the maternal pelvic inlet
How are anomalies of Müllerian duct fusion diagnosed
Screening tests
- Transvaginal or abdominal ultrasound
- Hysterosalpingography
Confirmatory test: MRI
What are the treatments of anomalies of Müllerian duct fusion
Surgical treatment is usually not recommended in the following situations:
- Another treatable cause of infertility co-exists
- The woman is asymptomatic
Metroplasty: reconstruction of the uterus
Septoplasty: a type of metroplasty that only involves resection of the septum in a separate uterus
What is Asherman syndrome
AKA Intrauterine adhesions
Endometrial adhesions or fibrosis
What is the aetiology of Asherman syndrome
Following uterine dilation or curettage (most common cause)
Postinflammatory (eg chlamydia)
What are the clinical features of Asherman syndrome
Usually asymptomatic Abnormal uterine bleeding Secondary amenorrhea Infertility Recurrent pregnancy loss Periodic abdominal pain
How is Asherman syndrome diagnosed
Progesterone withdrawal test: bleeding does not occur following progestin withdrawal given block of the outflow tract
Hysterosalpingography: honeycomb appearance of the uterus
Confirmatory test: hysteroscopy to directly visualise adhesions
How is Asherman syndrome treated
Hysteroscopic resection of the adhesions
Treatment is only indicated if patient is symptomatic
What is an imperforate hymen
A hymen without an opening
A congenital defect
Seen in 1:1000-2000 females
What is the pathophysiology of an imperforate hymen
Central cells of the Müllerian eminence in the urogenital sinus do not disintegrate → imperforate hymen → cryptomenorrhea at puberty (outflow tract obstruction leads to backup of menstrual blood) → hematocolpos (accumulation of blood in the vagina) and/or hematometra (accumulation of blood in the uterus)
What are the clinical features of an imperforate hymen
Asymptomatic before puberty: At birth, vaginal secretions accumulate → may be detected as a swelling in the introitus → spontaneous resolution
Primary amenorrhea with periodic lower abdominal pain
Possible urinary retention, frequency, dysuria
Possible palpable lower abdominal mass
Perineal examination: tense, bulging, bluish membrane in the vulva
How is an imperforate hymen diagnosed
Primarily a clinical diagnosis but imaging may be conducted to rule out transverse vaginal septum
How is an imperforate hymen treated
Excision of the imperforate hymen (hymenectomy)
What is agenesis of the upper vagina
A condition in which the vagina is abnormally closed or absent
Seen in 1/5000 female individuals
Caused by Müllerian agenesis
What is the pathophysiology of agenesis of the upper vagina
Agenesis or hypoplasia of the Müllerian duct → atresia of the upper-third of the vagina
Normally functioning gonads and female karyotype → normal development of secondary sexual characteristics (e.g., breast, pubic hair development)
Associated anomalies:
- Absent or malformed uterus and cervix (in almost all cases)
- Urological malformations (25–50% of cases): single kidney, pelvic kidney, horseshoe kidney
- Skeletal malformations (10–15% of cases)
What are the clinical features of agenesis of the upper vagina
Asymptomatic before puberty Primary amenorrhea Infertility Dyspareunia Perineal examination: vaginal dimple and a hymenal fringe
How is agenesis of the upper vagina diagnosed
Normal levels of LH, FSH, prolactin, estradiol, and testosterone
Ultrasound:
- Absent or malformed uterus (e.g., hemiuterus, rudimentary uterus)
- Normal ovaries
- Possible associated malformations of the kidneys or urinary tract
MRI to determine if functional endometrium is present
How is agenesis of the upper vagina treated
Vaginoplasty
What is the cause of agenesis of the lower vagina
Abnormal development of the sinovaginal bulbs and vaginal plate
What are the clinical features of agenesis of the lower vagina
Primary amenorrhea
Cyclic pelvic pain
How is agenesis of the lower vagina diagnosed
Vaginal dimple may be present on physical exam
Palpable abdominal mass due to distention of the upper vagina
Confirmatory tests: ultrasound or MRI:
- Normal ovaries, uterus, cervix, and upper vagina
- Measurement of the distance from introitus to obstruction
How is agenesis of the lower vagina treated
Surgical pull through procedure
What is the pathophysiology of transverse vaginal septum
Failure of recanalization of the Müllerian duct → transverse septum in the upper-third (45%), lower third (15–20%), and/or middle third (35–40%) of the vagina
Associated with cervical hypoplasia or absence
Cryptomenorrhea → hematocolpos
What are the clinical features of transverse vaginal septum
Asymptomatic before puberty Primary amenorrhea Infertility Periodic lower abdominal pain Possibly, palpable lower abdominal mass Perineal examination: normal vulva and external genitalia
How is transverse vaginal septum diagnosed
Transvaginal ultrasonography
MRI
How is transverse vaginal septum treated
First-line: nonsurgical dilation over 6–12 months using graduated vaginal dilators
Second-line: vaginoplasty
What is labial fusion
Partial or complete adhesion of the labia minora
Occurs in 2-5% of females up to 4 y/o
How common is transverse vaginal septum
1/70,000 females
What causes labial fusion
Absence of estrogen → predisposition to mild infection → local inflammation → raw surface epithelium of the labia minora → adhesions
In rare cases: trauma (sexual abuse), congenital defect
What are the clinical features of labial fusion
Usually asymptomatic
If external urethral opening is obstructed: recurrent attacks of UTI, vaginitis, vestibulitis
Perineal examination:
- A thin vertical midline fold in the perineum
- The labia, vaginal opening, and occasionally the urethral meatus are not visible.
How is labial fusion diagnosed
Primarily clinical diagnosis
How is labial fusion treated
Application of topical oestrogen
What is the start of menstruation called
Menarche
What is the cessation of menstruation
Menopause
What is meant by the term menses
Menstrual bleeding
What regulates the mentstrual cycle
A tightly regulated process in which the coordinated release of hormones from the hypothalamus, pituitary gland, and gonads produces a single mature oocyte. These hormones are controlled by positive and negative feedback loops.
What is amenorrhea
Menstrual cessation
No period
What is primary dysmenorrhea
Recurrent lower abdo pain shortly before or during menstruation (in the abscence of pathological findings that could account for those symptoms)
What is meant by abnormal uterine bleeding
AKA ABU
Increased frequency and/or volume of menstruation
What is meant by Premenstrual syndrome
Discomfort prior to the onset of menstruation that is accompanies by psychiatric, gastro, and/or near symptoms
What is an oocyte
An immature female germ cell that can undergo oogenesis to become an ovum.
How long is a normal menstrual cycle
24-38 days (28 days on average, with the first day of menstrual bleeding counted as day 1 of the cycle
First few years after menarche the cycles will be irregular due to immaturity of the hypothalamic-pituitary-gonadal axis
Cycles are longest at age 25-30, with younger and older individuals having shorter cycles
What is the epidemiology of primary dysmenorrhea
Prevalence up to 90%
Most common gynaecologic condition
Mainfiestes during adolescence (typically within 3 years of menarche)
What is the aetiology of primary dysmenorrhea
Not completely understood
Associated with risk factors:
- Early menarche
- Nulliparity
- Smoking
- Obesity
- Postive family history
What is the pathophysiology of primary dysmenorrhea
Increased endometrial prostaglandin (PGF2 alpha) production leads to vasoconstriction/ischemia and stronger, sustained uterine contractions (to prevent blood loss).
What are the clinical features of primary dysmenorrhea
Usually occurs during the first 1–3 days of menstruation
Spasmodic, crampy pain in the lower abdominal and/or pelvic midline (often radiating to the back or thighs)
Headaches, diarrhea, fatigue, nausea, and flushing are common accompanying symptoms.
Normal pelvic examination
How is primary dysmenorrhea diagnosed
Primary dysmenorrhea is a diagnosis of exclusion.
Rule out conditions that cause secondary dysmenorrhea (e.g., endometriosis).
How is primary dysmenorrhea treated
Symptomatic treatment: pain relief (e.g., NSAIDs), topical application of heat
Hormonal contraceptives (e.g., combined oral contraceptive pill, IUD with progestogen)
What is secondary dysmenorrhea
Recurrent lower abdominal pain shortly before or during menstruation that is due to an underlying condition
What is the epidemiology of secondary dysmenorrhea
May begin later in life than primary dysmenorrhea
Commonly affects female individuals ≥ 25 years of age
What is the aetiology of secondary dysmenorrhea
Uterine causes:
- Pelvic inflammatory disease (PID)
- Intrauterine device (IUD)
- Adenomyosis
- Fibroids (intracavitary or intramural)
- Cervical polyps
Extrauterine causes:
- Endometriosis
- Adhesions
- Functional ovarian cysts
- Inflammatory bowel disease
What are the clinical features of secondary dysmenorrhea
Depend on the underlying cause
Secondary dysmenorrhea should be suspected in the following cases:
- Abnormal pelvic examination (e.g., uterine size, cervical motion tenderness, adnexal tenderness, masses, vaginal/cervical discharge)
- The pain tends to get worse over time.
- No previous history of pain with menstruation
- Infertility (e.g., adhesions, endometriosis, PID)
- Irregular cycles
- Heavy menstrual flow (e.g., adenomyosis, fibroids, polyps)
- Dyspareunia or postcoital bleeding
- Partial or no response to therapy with NSAIDs and/or hormonal contraceptives
How is secondary dysmenorrhea diagnosed
Depend on the underlying cause Initial laboratory testing CBC with differential (rules out infection) Urinalysis (rules out UTIs) Other β-hCG (rules out ectopic pregnancy), Gonococcal/chlamydial swabs (rule out STDs and PID) Pelvic ultrasound
How is secondary dysmenorrhea treated
Treat the underlying cause
What is dyspareunia
A symptom of pain that occurs during or after sexual intercourse.
What is primary amenorrhea
The absence of menarche at 15 years of age despite normal development of secondary sexual characteristics
or
Absence of menses at 13 years of age in female individuals with no secondary sexual characteristics
What is the aetiology of primary amenorrhea
- Constitutional growth delay
- Hypogonadotropic hypogonadism
- Hypergonadotropic hypogonadism
- Anatomic anomalies
- Receptor and enzyme abnormalities
How is primary amenorrhea diagnosed
Pregnancy test
Check for secondary sexual characteristics and anatomical anomalies (physical examination, pelvic ultrasound):
- Uterus absent: Perform karyotyping and serum testosterone to investigate for male/female genotype and androgen sensitivity
- Uterus present: Test FSH and LH levels:
- -Exclude imperforate hymen, vaginal atresia, and transverse vaginal septum.
- -↑ FSH: primary ovarian insufficiency (e.g., Turner syndrome, Swyer syndrome, premature ovarian failure)
- -Normal or ↓ FSH: constitutional growth delay, hypogonadotropic hypogonadism
If galactorrhea is present:
–Check prolactin and TSH levels.
If symptoms of hyperandrogenism are present:
- Check serum testosterone and dehydroepiandrosterone sulfate (DHEA-S)
- -If high: Suspect an androgen-secreting tumor.
If blood pressure is high: Suspect congenital adrenal hyperplasia.
How is primary amenorrhea treated
Management of the underlying cause:
- anatomical anomalies - surgery
- Hypogonadism - hormone replacement therapy with oestrogens and progesterone
Goal of treatment is the progression of normal pubertal development
What is amenorrhea physiological
Before menarche
After menopause
During pregnancy
During lactation
What is the female athlete triad of functional hypothalmic amenorrhea
Low calorie intake/ strenuous physical activity
Low bone mineral density
Amenorrhea
What is abnormal uterine bleeding (AUB)
Formerly known as dysfunctional uterine bleeding
Defined as menstrual bleeding that is abnormal and/or irregular in frequency, duration and/or intensity
It may or may not be accompanied by dysmenorrhea
What is the aetiology of abnormal uterine bleeding
PALM -COEIN system
Structural causes (PALM):
- polyps
- adenomysosis
- leiomyomas and malignancy and hyperplasia
Nonstructual causes (COEIN):
- coagulopathy
- ovulatory dysfunction
- endometrial
- iatrogenic
- not otherwise classified
What is acute AUB
Episodic uterine bleeding, in a nonpregnant female individual of reproductive age, that is of sufficient volume to require intervention to prevent further blood loss
What is chronic AUB
Uterine bleeding of abnormal frequency, regularity, and/or volume that has persisted for > 6 months
How can AUB be classified
According to aetiology
AUB-C: coagulopathies
AUB-O: ovulation disorders (e.g., disorders of the hypothalamic-pituitary axis)
AUB-E: endometrial disorders
AUB-I: iatrogenic causes (e.g., estrogens, androgens, IUD)
AUB-N: not otherwise classified (e.g., uterine arteriovenous malformations, cesarean scar defect)
How is AUB diagnosed
Gynae history:
- Age of menarche
- Last menstrual period
- Cycle length and regularity
- Pregnancies
- FH
- Recent complaints
- Evaluation of possible causes guided by PALM-COEIN system
- Characteristics of abnormal bleeding (frequency, regularity, duration, volume)
Physical Exam:
- If acute bleed - ensure haemodynamic stability
- Pelvic exam- Assess the severity and source of the bleeding (exclude structural abnormalities, neoplasms and trauma)
- Swabs for microbiologic testing to rule out cervicitis due to gonorrhoea/ chlamydial infection
Pap smear:
- rule out cervical carcinoma
Initial lab testing:
- FBC - anaemia
- Platelet count, PT, PTT, rule out bleeding disorders
- B-hCG - rules out pregnancy
- Additional (TFTs, Prolactin, Serum iron)
Pelvic Ultrasound:
- To rule out structural anomalies
- Evaluation of endometrial thickness
Endometrial biopsy:
- Indications vary by age group and risk factor presence
- Postmenopausal w/ any uterine bleeding and/or endometrial thickness ≥ 4mm
- All >45y/o with frequent, heavy, and/or prolonged bleeding
- <45y/o with frequent, heavy and/or prolonged bleeding who are at high risk for endometrial cancer and/or have failed medical management
When is ovulation
Day 14 (counted from last menstrual period)
Where does fertilisation and therefore conception occur
In the fallopian tube
What is each stage of the fertilised egg during cell division in the fallopian tube
Zygote to morula to blastocyst which then enters the uterine cavity
How many cells in a blastocyst
64 cells
What day does the blastocyst implant in the uterine cavity
23 (counted from last menstrual period), starting metal maternal dialog
What is the most common site for an ectopic pregnancy implantation
Ampulla of the Fallopian tube
What happens at implantation
Blastocyst implants causes release of hCG which stimulates the ovary to produce progesterone
How do HCG levels rise
Rapidly up to 10 weeks, then plateau and potentially drop
How is hCG used in diagnosis
Basis of pregnancy test
Can be detected in serum and urine 4 weeks after last menstrual period, so just 2 weeks after conception
Urine +ve when conc reaches 25IU/ml
What is progesterone
Main pregnancy hormone
Modifies maternal physiology:
-cardio (increase in HR, stroke volume, so cardiac output increase, BP drops)
-resp (less lung capacity, so SOB, may make pathology difficult to identify)
-Uterine quiescence (relaxation)
-Immune system (immuno suppressive - so not to reject baby, but can increase infection risk) (can be a problem in those already immunosuppressed eg HIV)
-smooth muscle relaxation (constipation, UTI - urinary stasis)
Can be given progesterone supplementation to mothers with late miscarriage past 20 weeks previously, as will often improve current pregnancy outcome
How quickly does the foetus grow in the first trimester
Doubles in size every week from 6 until 12 weeks gestation
What can be seen in a pregnancy transvaginal ultrasound at what weeks
4-5 weeks: gestational sac 6mm
5-6 weeks: yolk sac
6 weeks: foetal pole 5mm
6.5-7 weeks: foetal heart activity
8 weeks: limb buds, foetal movements
How is a pregnancy dated
Crown-rump length of foetus
What determines the growth of the foetus
Intrinsic factors:
- Maternal
- height and weight (bigger mum, bigger baby)
- parity (bigger baby the more pregnancies)
- ethnic group
- Foetal
- sex (boys bigger)
- genes/inherited conditions
- multiple pregnancies (twins etc will be smaller than equivalent single foetus)
Extrinsic factors:
- Maternal:
- social class
- nutritional status
- environment (high altitude, smaller baby)
- pre-existion disease
- pregnancy-related disease
- – hypertension (small baby), diabetes (large baby)
- Fetal
- nutrition (placenta)
- Teratogenic
- Infective
- – viral (rubella, CMV)
What is intera uterine growth restriction
When the baby is small for gestational age, not growing as expected
What fetal measurements are taken on ultrasound for foetal growth
BPD: biparietal diameter
HC: Head circumference
AC: Abdominal circumference (T12 level)
FL: Femur length
This is then plotted on percentile graphs
Serial scans needed, one scan cannot prove whether constitutionally small or IUGR.
However, can compare the centile plotting of head circumference and abdominal circumference, and if AC
What does the biophysical profile on ultrasound look at
Indicator of how the baby is coping
Fetal breathing movements
Fetal movements
Fetal tone
Amniotic fluid volume
How is placental function assessed
DOPPLER to assess blood flow in foetal arteries
DOPPLER doesn’t measure blood flow directly but this is inferred from the wave forms on the ultrasound screen to produce the pulsatility index and resistance index
If high PI and RI then sign of placental insufficiency
Alterations in foetal blood flow can be an eraly indication of foetal compromise
What is a high risk pregnancy
A high risk pregnancy is one in which the probability of an adverse outcome in the mother and/or baby is greater than that for a pregnant woman in general
A pregnancy requiring medical involvement
Who is at high risk in pregnancy
Maternal conditions Social factors Obstetric issues in previous pregnancy Problems in this pregnancy Problems during labour
What maternal conditions canmake a pregnancy high risk
Obesity
Diabetes
Hypertension
Chronic disease (renal, autoimmune, respiratory..)
Infections
Previous surgery
VTE (100x more likely for VTE in this pregnancy if previous VTE)
What social factors can make a pregnancy high risk
Teenage pregnancy Maternal age >40 High parity and low interpregnancy interval (> risk of haemorrhaging) Poor socioeconomic conditions Alcohol intake Substance abuse
What obstetric issues in previous pregnancy can make a pregnancy high risk
Caesarean section Preterm delivery Recurrent miscarriage (>/=3) Stillbirth Pre-eclampsia Gestational diabetes Third degree tear
What is a third degree tare
Anal sphincter
3a <50% external AS involved
3b <50% external AS involved
3c internal AS involved
What is a first degree tear
Vaginal sphincter
What is a second degree tear
Tear of perineal muscles
What problems in this pregnancy can make a pregnancy high risk
Multiple Pregnancy Small for gestation age Placenta praevia (low-lying placenta) (has to have a c-section) (will bleed a lot in surgery) Gestational diabetes Pre-eclampsia
What problems during labour can make a pregnancy high risk
Meconium stained liquor Blood stained liquor Worrying features on CTG Need for oxytocin infusion Lack of progress
Who provides the care to pregnant women
Midwife / GP-led - UNCOMPLICATED PREGNANCY
Consultant-led shared care - HIGH RISK PREGNANCY
What is the risk of scar dehiscence in viginal birth after csection (VBAC)
1:200 in spontaneious labour
2-3:200 in medically induced labour
WHat is the success rate of VBAC
75% in spontaneous labour with no previous vaginal deliveries
90% in spontaneous labour with previous vaginal deliveries
Which mother’s who have had a previous C section should not attempt VBAC
Scarring in upper uterine segment:
- classical caesarean incision
- exteme prematurity/ foetal abnormality
- placential site issues
- uterine abnormality/ fibroid position
- J or inverted T incision
- usually due to difficulty during previous delivery
Other previous surgical complications Multiple previous C sections Short inter-pregnancy interval (<1 year) Increased risk of obstructed labour - previous history -BMI -Foetal vs maternal size
Don’t attempt VBAC if not willing for monitored hospital birth
Where is bleeding likely to be coming from in intermenstrual bleeding
Endometrium
Where is bleeding likely to be coming from in post coital bleeding
Cervix or in vagina
Where is bleeding likely to be coming from in post menopausal bleeding
12 months free of period,
Red flag for potential endometrial cancer
Most common cause atrophic vaginitis
What is dyspareunia
Pain during intercourse
Can be superficial or deep
What is GnRH
Gonodotrophin Releasing Hormone
Decapeptide
Secreted by mid basal hypothalamic neurons
Hourly pulses
Transported to pituitary via hypophyseal portal blood system
What affects GnRH secretion
Bereavement Anxiety Time zone Day/night duty Exercise Weight loss/gain
What is the role of FSH
AKA Follicle stimulating hormone
Stimulates follicular activity, thus promoting estradiol production from granulosa cells
What is the role of LH
AKA Luteinising hormone
Triggers release of egg from dominant follicle
Promotes development of the corpus luteum and the production of progesterone
What is the journey of a follicle leading to ovulation
Primordial follicle Primary/preantral follicle Secondary/antral follicle Provulatory follicle Ovulation
What is the endometrium
Lining of the uterus where a pregnancy will implant and be nourished
What is the proliferative phase
Oestrogen (estradiol E2) causes endometrial proliferation Endometrium thickens Increase in stromal cells Increase in glands, blood vessels By ovulation endometrium 2-3mm thick
Why can oestrogen be dangerous
If allowed to continually produce and so cause continuous proliferation of the endometrium, unopposed by progesterone, it can cause cancer
What is the secretory phase
Progesterone dominant hormone causing: -increasing in secretion -increase in lipids and glycogen -increase in blood supply -endometrium 4-6mm thick Optimal conditions for implantation of fertilised egg (stable, vascular, nutrient rich)
What causes period bleeding commencement each cycle
Drop in prgesterone due to death of corpus luteam
What is high spinnbarkeit
Stringy and runny muscus type midcycle, to facillitate sperm access at ovulation
Where is mucus in the cervix produced
Columnar glands
How is the mucus in the luteal phase of the cycle
Tenacious and inelastic
To prevent microbial ingress so protects the developing embryo
This mucus plug is critical to pregnancy (Coreo amnioitis)
How long is the luteal phase
A constant 14 days in length
What is menopause
Is the last menstrual period
Average age at menopause is ~51 years
What is postmenopause
Is the time after complete cessation of menstruation
Can only be known with certainty after 12 months of amenorrhoea
Or 6 months with high levels of FSH and LH
What is primary ovarian insufficiency
Menopause before age of 40 y/o
What is HRT
Hormone replacement therapy
What symptoms are suggestive of pelvic inflammatory disease
Recent onset (usually <30 days)
Lower abdominal pain – often bilateral
Abnormal vaginal discharge – often purulent
Deep dyspareunia
Abnormal vaginal bleeding including IMB, PCB & menorrhagia
Secondary dysmenorrhoea
What are the risk factors for endometrial cancer
Obesity PCOS Type 2 diabetes Tamoxifen therapy Lynch syndrome
How is abnormal uterine bleeding managed
Attain haemodynamic stability
Pharmacological:
- Acute AUB:
- High dose IV conjugated equine oestrogen
- Alternatives: multidose regimens of Oral contraceptive pills or oral progestins, as well as tranexamic acid
- Oculatory Bleeding:
- OCP, Progestin
- NSAIDs
- Tanexamic acid
- Anovulatory bleeding:
- Progestin PO for 10 days or as an IUD
- OCPs
Surgical:
- Uterine dilation and curettage with concomitant hysteroscopy
- Endometrial ablation
- Trancatheter uterine artery embolisation
- Hysteroscopy
- Hysterectomy
What are the indications for surgical intervention in AUB
Severe bleeding/ hemodynamic instability
Patient unresponsive to hormonal treatment
Hormonal treatment contraindicated (e.g., breast cancer, endometrial cancer)
Underlying medical condition requiring surgical repair
What are the signs and symptoms of PMS
Onset of symptoms 5 days before menstruation
Pain: dyspareunia, breast tenderness, headache, back pain, abdominal pain
Gastrointestinal changes: nausea, diarrhea, changes in appetite (food cravings)
Bloating and weight gain
Tendency to oedema formation
Neurological: migraine, increased sensitivity to stimuli
Psychiatric: mood swings, drowsiness, lethargy, exhaustion, depression, anxiety, aggressiveness, social withdrawal
How is PMS diagnosed
Diagnosis is based on history and self-assessment
Preexisting endocrine (e.g., thyroid disorders) and psychiatric (e.g., major depressive disorder) conditions should be ruled out.
WHat is PMS
The onset of severe discomfort or functional impairment prior to menstruation
What is Premenstrual dysphoric disorder
Aka PMDD
Severe affective symptoms and behavioural changes that cause clincially significant disturbance to daily life
What are the diagnostic criteria for PMDD
Present up to 7 days prior to the onset of menstruation for the majority of cycles within one year
≥ 5 symptoms that are marked and/or persistent (e.g., depressed mood, anxiety, anger, affective lability, sleep disturbances, change in appetite, pain, headache)
Significant interference in daily life (work, home, social activities, interpersonal relationships)
What are the diagnostic criteria for PMS
Present in the 5 days prior to the beginning of menstruation for at least 3 consecutive cycles
End within 4 days after the beginning of menstruation
Interfere with normal daily life activities
How is PMS treated
Lifestyle changes can be beneficial (e.g., regular exercise, healthy diet, avoiding individual triggers like alcohol, caffeine, or nicotine).
First-line treatment
- NSAIDs (e.g., naproxen)
- OCPs
- SSRIs (e.g., fluoxetine) in the case of severe PMS and PMDD
Dietary supplements: reduce symptoms and improve mood swings
- Calcium (1,200 mg/day) [16]
- Vitamin E
- Vitamin D
In the case of water retention/bloating:
- Diuretics (e.g., spironolactone)
- Magnesium
What is Mittelschmerz
Physiological preovulatory pain in female individuals of reproductive age
Also referred to as ovulatory or midcycle pain
How common is Mittelschmerz
~40% of females of reproductive age
What is the aetiology of Mittelschmerz
Enlargement and rupture of the follicular cyst and contraction of Fallopian tubes during midcycle ovulation leading to transient peritoneal irritation from follicular fluid.
WHat are the clinical features of Mittelschmerz
Recurrent unilateral lower abdominal pain (can mimic appendicitis)
Pain occurs during midcycle in individuals with regular menses.
Dull and achy pain which can become cramp-like
Can last up to 3 days
Physical examination: lower abdominal pain on palpation
How is Mittelschmerz managed
With NSAIDs as needed
What is PCOS
One of the most common endocrine disorders in women
It is characterized by hyperandrogenism (which primarily manifests as hirsutism, acne, and, occasionally, virilization), oligoovulation/anovulation, and/or the presence of polycystic ovaries.
What is teh prevalence of PCOS
6-12% of women in their reproductive years in the US
What is the most common cause of Hyperandrogenism
PCOS
What are the clinical features of PCOS
Menstrual irregularities
- Primary or secondary amenorrhea
- Oligomenorrhea
- Menorrhagia
- Infertility or difficulties conceiving
Insulin resistance and associated conditions
- Metabolic syndrome (especially obesity) → ↑ risk of sleep apnea
- Nonalcoholic fatty liver disease
Skin conditions
- Hirsutism
- Androgenic alopecia
- Acne vulgaris
- Oily skin
- Acanthosis nigricans
Psychiatric conditions
- Depression
- Anxiety disorders
How does PCOS present macroscopically
Multiple, brown cysts arranged in a circular pattern in the subcapsular region of the ovary
Cysts are relatively small and of approximately the same size.
How does PCOS present microscopically
Ovarian hypertrophy with thick capsule Stromal hyperplasia and fibrosis Multiple enlarged cystic follicles Hyperluteinized theca cells Decreased granulosa cell layer
What are the differentials for hyperandrogenism
PCOS Nonclassic congenital adrenal hyperplasia Congenital adrenal hyperplasia Cushing disease Hypothyroidism Hyperprolactinaemia Androgen secreting tumor Acromegaly Ovarian hyperthecosis Placental aromatase deficiency Drug induced (eg exogenous steroid and androgen intake)
What is hyperandrogenism
A state of excess androgen levels that causes symptoms such as growth of facial hair, deepening of the voice, and male-pattern baldness
What are the clinical features of hyperandrogenism
Virilization: the appearance of male secondary sexual characteristics in a female individual
Hirsutism: excessive male pattern hair growth (e.g., chin, upper lip, mid-sternum, abdomen, back, buttocks)
Male-pattern hair loss
Acne
Increased muscle mass
Voice deepening
Clitoromegaly
Rapid onset of virilization is suggestive of exogenous androgen intake or androgen-secreting tumors
Manifestations of the underlying condition
How is hyperandrogenism diagnosed
Laboratory tests to identify hyperandrogenemia:
↑ Serum total testosterone
↓ SHBG
Free androgen index
Investigate for the underlying cause.
How is hyperandrogenism treated
Medication to suppress or block androgen and manage symptoms of virilization
OCP
Antiandrogen drugs (e.g., spironolactone, finasteride)
Treat the underlying cause (e.g., surgery for androgen-secreting tumors).
What is the Rotterdam criteria
Criteria used to diagnose PCOS
Must have 2 or more of the following (and have excluded other anocrinological conditions)
-Oligoovulation and/or anovulation
-Hyperandrogenism (based on clinical features or laboratory studies): Examine patients for signs of acne, alopecia, and hirsutism; obtain laboratory studies as needed. [6]
-Enlarged and/or polycystic ovary on ultrasound
– Ovarian volume ≥ 10 mL
– AND/OR the presence of multiple cystic follicles measuring 2–9 mm (string-of-pearls appearance) in one or both ovaries [10]
What are the laboratory studies for PCOS
Confirm hyperandrogenism: -Obtain in all women with clinical features of PCOS, even if features are minimal or unclear: ↑ Testosterone ↑ Androstenedione ↑ dehydroepiandrosterone sulfate
Rule out differential diagnoses: e.g., pregnancy, endocrine disorders
A clinical picture of hyperandrogenism fulfills a diagnostic criterion of pcos, even if serum androgen levels are normal
An elevated LH (with LH:FSH ratio > 2:1) is a characteristic finding in most patients with PCOS but not necessary for diagnosis.
Identification of cystic follicles is not mandatory to diagnose PCOS
What screening must those with PCOS undergo
Patients with PCOS are at risk of serious comorbidities, even at a young age.
It is important to screen for these at the first visit and at regular intervals.
Metabolic screening and monitoring:
- Measure weight, height, and waist circumference; calculate BMI.
- For patients with elevated BMI: Obtain a fasting lipid profile and screen for symptoms of obstructive sleep apnea.
- Check blood pressure
- Assess glycemic status
Mental health and quality of life:
-Screen for anxiety, depression, and psychosexual dysfunction.
How is PCOS treated
Weight loss
Combined oral contraceptives:
- Indication: first-line treatment for hyperandrogenism and/or menstrual cycle abnormalities
- Additional benefits:
- ↓ Endometrial hyperplasia → ↓ risk of endometrial carcinoma
- ↓ Menstrual bleeding
- ↓ Acne
- Treatment of hirsutism
Metformin
- improves menstrual irregularities, metabolic outcomes, and weight (especially when combined with lifestyle modifications)
Antiandrogens:
- Controversial role
- Examples: spironolactone, finasteride, flutamide
- Indications: can be considered for treatment of hirsutism and androgen-related alopecia in patients unable to take or tolerate COCs
Additional interventions:
- Antiobesity medications
- Bariatric surgery, may be considered on a case-by-case basis.
How should patients with PCOS, planning to conceive, be treated
Letrozole:
- First-line therapy for ovulation induction
- Improves pregnancy and live birth rates in patients with anovulatory infertility with no other causes
- Mechanism of action: aromatase inhibition reduces estrogen production, stimulating FSH secretion and inducing ovulation
Clomiphene:
- Alternative to letrozole
- May be preferred over metformin monotherapy in obese women with anovulatory infertility
- Mechanism of action: inhibits hypothalamic estrogen receptors → disruption of the negative feedback mechanism governing oestrogen production → ↑ pulsatile secretion of GnRH → ↑ FSH and LH → stimulation of ovulation
Exogenous gonadotropins:
- The low-dose regimen is the second-line treatment for ovulation induction.
- Agents:
- Exogenous FSH
- Human menopausal gonadotropin
- Indication: typically used if first-line therapies are unsuccessful; occasionally used as first-line if the drug and monitoring requirements are accessible
Metformin:
- Can be used as second-line monotherapy for fertility treatment.
- Combination with clomiphene may increase pregnancy rates, especially in obese women.
- First-line therapy for insulin resistance
Additional fertility interventions:
- Laparoscopic ovarian drilling:
- a laparoscopic procedure in which ovarian tissue is reduced with a laser beam or surgical needle to decrease its volume and androgen production
- this hormonal shift can induce FSH secretion and improve ovarian function in patients with polycystic ovary syndrome.
- second-line treatment for ovulation induction; can be performed as a first-line treatment if other indications for laparoscopy exist
In vitro fertilization: can be offered as third-line therapy
Management of other PCOS manifestations
- Hirsutism:
- Nonpharmacological therapy is first-line (e.g., electrolysis, light-based hair removal via laser or photoepilation)
- Acne:
- Consider topical therapies (e.g., benzoyl peroxide, topical antibiotics)
What are potential complications of PCOS
Cardiovascular disease Type 2 diabetes mellitus Increased cancer risk (before menopause) -Endometrial cancer -Ovarian cancer -Pancreatic cancer -Kidney cancer -Endocrine cancers (except thyroid) Increased miscarriage rate
What is perimenopause
Definition: the time period from the first instance of climacteric symptoms caused by fluctuating hormonal levels to one year after menopause
Duration: The average length of perimenopause is 4 years.
What is premenopause
Definition: the time period from the first occurrence of climacteric irregular menstruation cycles to the last menstrual period
Onset: usually 45–55 years of age
Characterized by increasingly infrequent menstruation
At what age does the menopause occur
~49–52 years (earlier in smokers)
What is postmenopause
The time period beginning 12 months after the last menstrual period
What is the pathophysiology of menopause
Numerical depletion of ovarian follicles with age → ↓ ovarian function → ↓ estrogen and progesterone levels → loss of negative feedback to the gonadotropic hormones → ↑ GnRH levels → ↑ levels of FSH and LH in blood (hypergonadotropic hypogonadism) → ↑ frequency of anovulatory cycles → ovarian function eventually stops permanently
What are the clinical features of menopause
HAVOCS:
- Hot flashes/ Heat intolerance
- Atrophy of Vagina
- Osteoporosis
- Coronary artery disease
- Sleep impairment
Irregular menses to complete amenorrhea
Autonomic symptoms:
- Hot flushes
- Vertigo
- Headache
Mental symptoms:
- Sleep impairment
- Depressed mood
- Mood swings
- Anxiety
- Irritability
- Loss of libido
Atrophic features (result from an age-related drop in oestrogen levels)
- Breast tissue atrophy (tenderness and reduced size)
- Vulvovaginal atrophy
- Urinary atrophy
- urinary incontinence
- dysuria
- urinary frequency
- urgency
- increased UTIs
- Osteoporosis
Weight gain and bloating
Hirsutism (due to relative increase in androgens
Increased risk of Coronary artery disease
What is a surgical menopause
Due to removal of ovaries (commonly after hysterectomy with bilateral salpingo-oophorectomy)
How is menopause diagnosed
Diagnosis is usually clinical. However, certain laboratory tests may help confirm the onset/presence of perimenopause: -↓ Estrogen -↓ progesterone -↓ inhibin B -↑↑ FSH -Testosterone and prolactin levels are within normal ranges. -Vaginal pH > 4.5 -Lipid profile: -- ↑ total cholesterol -- ↓ HDL
When is menopause treatment indicated
Treatment is not warranted for all women approaching or undergoing menopause, as it is a normal aging process. Treatment may be considered in the following cases: Symptoms are severe enough to infringe significantly on functional capacity, and hence affect quality of life. Premature menopause Surgical menopause (e.g., post-oophorectomy)
What is HRT
Short term treatment of menopausal symptoms
Types:
Estrogen therapy: for women who have had a hysterectomy
Estrogen plus progestin therapy: for women with a uterus
Routes: oral, transdermal
Risks
Cancer
Unopposed estrogen can result in endometrial hyperplasia → increased risk of endometrial cancer
Estrogen plus progestin therapy → increased risk of breast cancer
Cardiovascular disease: coronary heart disease, deep vein thrombosis, pulmonary embolism, stroke
Gallbladder disease
Stress urinary incontinence
Contraindications
Undiagnosed vaginal bleeding
Pregnancy
Breast cancer/endometrial cancer
Chronic liver disease
Hyperlipidemia
Recent DVT/stroke
Coronary artery disease
What are the non-hormonal therapies available for menopause treatment
Non-hormonal therapy is used to treat menopausal vasomotor symptoms in women who do not want to use hormonal medications or who have contraindications for HRT.
Selective estrogen receptor modulators:
- tamoxifen
- ospemifene
- raloxifene
Paroxetine:
-for vasomotor symptoms (i.e., hot flashes)
Clonidine and/or gabapentin
What is the definitition of premature menopause
Permanent cessation of menses before the age of 40
What causes premature menopause
Idiopathic
Primary ovarian insufficiency
Bilateeral oophorectomy
What is ovarian insufficiency
Failure of adequate ovarian function (endocrine as well as reproductive) before the age of 40, which often leads to premature menopause
What is primary ovarian insufficiency
Ovarian insufficiency despite adequate gonadotropin stimulation (previously called premature ovarian failure)
What causes primary ovarian insufficiency
Idiopathic (90% of cases)
Genetic disorders associated with ovarian hypoplasia, especially in women < 30 years (e.g., Turner syndrome, Swyer syndrome, androgen insensitivity syndrome, adrenogenital syndrome, fragile X syndrome)
Autoimmune diseases (e.g., autoimmune lymphocytic oophoritis, Hashimoto thyroiditis, Addison disease, type I diabetes mellitus, pernicious anemia)
Toxins: Smoking is a major risk factor.
Iatrogenic: radiation and/or chemotherapy, prolonged GnRH agonist therapy, induction of multiple ovulation in infertility treatment
Infectious diseases (e.g., measles, mumps, tuberculosis of the genital tract)
What is the pathophysiology of premature ovarian insufficiency
Follicular dysfunction or depletion → ↓ estrogen levels → reduced feedback inhibition of estrogen on FSH and LH → ↑ FSH and LH (usually FSH > LH)
What are the clinical features of premature ovarian insufficiency
Climacteric symptoms such as vaginal dryness, night sweats, hot flashes, dyspareunia, and irritability
Abnormal/irregular bleeding pattern that can progress to secondary amenorrhea or permanent cessation of menstruation
Infertility or reduced fertility (Pregnancy is possible via in vitro fertilization.)
How is premature ovarian insufficiency diagnosed
Confirmed by two high FSH levels (> 30–40 mIU/mL) and two low estradiol levels (< 50 pg/mL) at least 1 month apart after > 3 months of menstrual irregularities in a woman under age 40
Further tests help determine the underlying cause (e.g, karyotyping, thyroid function)
How is premature ovarian insufficiency treated
Hormone replacement therapy
Treatment of underlying causes
What is secondary ovarian insufficiency
Ovarian insufficiency due to inadequate stimulation of the ovaries by the hypothalamus and/or pituitary
What is the definition of postmenopausal bleeding
Any vaginal bleeding that occurs after menopause in women who are not taking HRT or any unscheduled bleeding in women who are taking HRT
What causes postmenopausal bleeding
Endometrial or vulvovaginal atrophy, submucous leiomyomas, and endometrial polyps are among the most common causes of postmenopausal bleeding.
Approx. 10% of cases of postmenopausal bleeding are due to endometrial cancer
What is pelvic organ prolapse
AKA POP or Female genital prolapse
The protrusion of bladder, rectum, intestines, uterus, cervix, or vaginal apex into the vaginal vault due to decreased pelvic floor support.
What is a partial or subtotal prolapse
Pelvic organs are only partially outside the vaginal opening
What is a total prolapse
Pelvic organs are everted and located outside the vaginal opening
What is the endopelvic fascia
The anatomy which suppots the pelvic floor and consists of:
- Uterosacral ligament complex (suspends the uterus and vaginal apex from the sacrum and lateral pelvis)
- Paravaginal attachments
- Perineal body, perineal membrane, and the perineal muscles
What are the specific sites of prolapse
Vaginal wall prolapse:
- Anterior vaginal wall prolapse: herniated anterior vaginal wall, which is often associated with a cystocele (descent of the bladder) or urethrocele (descent of the urethra); can be due to weakness of the pubocervical fascia
- Posterior vaginal wall prolapse: herniated posterior vaginal wall, which is associated with a rectocele (descent of the rectum) or enterocele (herniated section of the intestines); can be due to weakness of the rectovaginal fascia
Uterine prolapse: descent of the uterus
Vaginal vault prolapse: descent of the apex of the vagina
Apical compartment prolapse: herniated uterus, cervix, or vaginal vault
Uterine procidentia: protrusion of all vaginal walls or cervix beyond the vaginal introitus
Who is most likely to have POP
Common disorder in older women
What causes POP
POP is due to an insufficiency of the pelvic floor muscles and the ligamentous supportive structure of the uterus and vagina, which may be caused by:
- Multiple vaginal deliveries and/or traumatic births (greatest risk factor)
- Low estrogen levels (e.g., during menopause)
- Increased intraabdominal pressure (e.g., obesity, cough related to chronic lung disease and/or smoking, ascites, pelvic tumors, constipation)
- Previous pelvic surgery (e.g., hysterectomy)
- Congenital connective tissue disorders
- Diabetes mellitus
What are the clinical features of POP
Feeling of pressure on or discomfort around the perineum (“sensation of vaginal fullness”)
Lower back and pelvic pain (may become worse with prolonged standing or walking)
Rectal fullness, constipation, incomplete rectal emptying
Prolapse of the anterior (most common) or the posterior vaginal wall:
- Occurs at rest and with increased abdominal pressure
- Possibly with excessive vaginal discharge on inspection, bimanual examination, and speculum examination of the patient in lithotomy position
Weakened pelvic floor muscle and anal sphincter tone
What is the Pelvic Organ Prolapse Quantitation system
AKA POP-Q
Stage 0: no prolapse
Stage 1: The most distal portion of prolapse is more than 1 cm above the level of the hymen.
Stage 2: The most distal portion of prolapse is 1 cm or less proximal or distal to the hymenal plane.
Stage 3: The most distal portion of prolapse is more than 1 cm from the hymenal plane but no more than 2 cm less than the vaginal length.
Stage 4: The vagina is completely everted or uterine procidentia has occurred.
What are the differentials of POP
Elongation of the cervix
Urethral diverticulum
Pelvic floor dysfunction
What is urethral diverticulum
A distinct outpouching of the urethral mucosa most often located posterolaterally in the mid and distal two-thirds of the urethra
What is the aetiology of urethral diverticulum
Acquired (most common):
- Recurrent infection of the periurethral glands
- Pelvic trauma (particularly involving the vagina, bladder, or urethra)
- Gynecological surgery, periurethral procedures
- Vaginal delivery
Congenital
What are the clinical features of urethral diverticulum
Dysuria
Dyspareunia
Urinary incontinence (particularly, postvoid dribbling of urine)
Tender anterior vaginal wall mass during pelvic examination
How is urethral diverticulum diagnosed
MRI
Transvaginal ultrasound if MRI is not available/feasible
Urinalysis to evaluate for other conditions (e.g., urinary tract infection or malignancy)
What is a skene dust cyst
A retention cyst that results from obstruction, accumulation of fluid, and cystic dilation of the ducts that drain the paraurethral glands.
Manifests with dysuria, dyspareunia, and urinary overflow incontinence.
Pelvic examination typically shows masses located just lateral to the external urethral meatus.
How is urethral diverticulum treated
Conservative management
- Indicated for individuals with minor symptoms
- Manual compression of the suburethral mass after voiding
Surgery
- Indicated for individuals with persistent symptoms, urinary calculi in the diverticulum, or suspicion of malignancy
- Transvaginal diverticulectomy: is a preferred procedure
What is pelvic floor dysfunction
Inability to relax and coordinate pelvic floor muscles correctly in order to urinate and/or have bowel movements
What are the clincial features of pelvic floor dysfunction
Urinary incontinence, urgency, and/or dysuria
Fecal incontinence
Dyssynergic defecation
Dyspareunia
Lower back or pelvic pain
Feeling of pressure on the pelvic region or rectum
Pelvic muscle spasms
How is pelvic floor dysfunction diagnosed
Clinical features and physical examination
Pelvic ultrasound
Urodynamic studies
Anorectal manometry
How is pelvic floor dysfunction treated
Pelvic floor muscle training (e.g., Kegel exercises) and physical therapy
Biofeedback and electrical stimulation: probes or electrodes are placed externally or inserted into the vagina or rectum to stimulate the pelvic floor muscles
Stool softeners and muscle relaxants
How is pelvic organ prolapse treated
Conservative:
- First line
- Insertion of a vaginal pessary to support the pelvic organs:
- A silicone or latex device that is inserted into the vagina
- Pessary insertion is not a long-term treatment!
- Reduction of modifiable risk factors (e.g., avoid smoking to prevent a chronic cough, weight loss, prevent constipation)
- Kegel exercises: pelvic floor muscle training (also as a preventive measure)
Surgery:
- Indicated for symptomatic prolapse if conservative treatment fails or the patient declines it
- Obliterative surgery: colpocleisis in which the vagina is closed off or narrowed to provide more support for pelvic organs.
- Reconstructive surgery (abdominal or vaginal approach): to restore the original position of the descended pelvic organs
- Sacrocolpopexy (with vaginal vault suspension and hysterectomy): fixation of the vaginal apex to the sacrum for the repair of apical or vaginal vault prolapse, with suspension and hysterectomy
- Suspension techniques: prolapsed organ is fixated or suspended using native tissues such as the endopelvic fascia, iliococcygeus muscle, uterosacral ligament, or sacrospinous ligaments.
- Colporrhaphy: reinforcement of the anterior or posterior vaginal wall for the repair of cystocele or rectocele
- Sacrohysteropexy: fixation of the cervix to the sacrum for the repair of uterine prolapse
What are potential complications of POP
Pressure ulcers with hemorrhage Ascending infections Urinary disorders Stress incontinence - "Masked" urinary incontinence - Obstructive uropathy Defecation disorders (e.g., constipation or fecal incontinence if the anal sphincter is weakened) Sexual dysfunction Surgical complications (e.g., recurrence)
What is vulvovaginitis
A large variety of conditions that result in inflammation of the vulva and vagina.
What causes infectious vulvovaginitis
Common causes of infectious vulvovaginitis:
- Bacterial vaginosis
- Vaginal yeast infection
- Trichomoniasis
- Aerobic vaginitis
Other causes of infectious vulvovaginitis:
- Gonorrhea
- Chlamydial genitourinary infection
- Enterobius vermicularis (especially in prepubescent girls)
- Scabies (seven-year itch)
- Pediculosis pubis (crabs, pubic lice)
What pathogen is involved in bacterial vaginosis
Gardnerella vaginalis (a pleomorphic, gram-variable rod)
What is the pathophysiology of BV
Lower concentrations of Lactobacillus acidophilus lead to overgrowth of Gardnerella vaginalis and other anaerobes, without vaginal epithelial inflammation due to absent immune response
What are the risk factors for BV
Sexual intercourse (primary risk factor, but it is not considered an STD)
Intrauterine devices
Vaginal douching
Pregnancy
What are the clinical features of BV
Commonly asymptomatic
Increased vaginal discharge, usually gray or milky with fishy odor
Pruritus and pain are uncommon
How is BV diagnosed
Diagnosis is confirmed if three of the following Amsel criteria are met:
Clue cells
- Vaginal epithelial cells with a stippled appearance and fuzzy borders due to bacteria adhering to the cell surface
- Identified on wet mount preparation: A sample of vaginal fluid/discharge is transferred to a slide and mixed with normal saline. The slide is then examined under a microscope.
Vaginal pH > 4.5
Positive Whiff test: an intensified fishy odor after adding 1–2 drops of 10% potassium hydroxide to a sample of vaginal fluid
Thin, homogeneous gray-white or yellow discharge that adheres to the vaginal walls
How is BV treated
If asymptomatic: reassurance; often resolves without treatment
If symptomatic
- First-line: oral metronidazole
- Alternative: topical metronidazole or clindamycin
Oral probiotics
What are potential complications of BV
Acquisition of STDs (e.g., HSV2, HIV, trichomonas, gonorrhea, and chlamydia infection)
Miscarriage and spontaneous abortion
Preterm delivery
Postpartum endometritis
What is the ABCDEFG acronym for BV
Amsel criteria
Bacterial vaginosis
Clue cells
Discharge (gray or milky)
Electrons (pH of vaginal secretions is alkaline)
Fishy odor of discharge
Gestation (increased risk for miscarriage)
All are the most important features of bacterial vaginosis.
What pathogen is involved in vulvovaginal candidiasis (aka vaginal thrush)
Primarily Candida albicans
in immunosuppressed patients also Candida glabrata
What is the pathophysiology of vulvovaginal candidiasis
Overgrowth of C. albicans
Can be precipitated by the following risk factors:
- Pregnancy
- Immunodeficiency, both systemic (e.g., diabetes mellitus, HIV, immunosuppression) and local (e.g., topical corticosteroids)
- Antimicrobial treatment (e.g., after systemic antibiotic treatment)
What are the clinical features of vulvovaginal candidiasis
White, crumbly, and sticky vaginal discharge that may appear like cottage cheese and is typically odorless
Erythematous vulva and vagina
Vaginal burning sensation, strong pruritus, dysuria, dyspareunia
How is vulvovaginal candidiasis diagnosed
Pseudohyphae on wet mount with potassium hydroxide (KOH)
Vaginal pH within normal range (4–4.5)
How is vulvovaginal candidiasis treated
Recommended regimens: topical azole (e.g., miconazole, clotrimazole, butoconazole) OR single-dose oral fluconazole
Recommended in pregnant women: topical azole OR nystatin pessary (where available)
What pathogen is involved in Trichomoniasis
Trichomonas vaginalis
Anaerobic, motile protozoan with flagella
Does not encyst and, therefore, does not survive well outside the human body
Under micrscope wiggles its little tail
How is TV transmitted
Sexually
What are the clinical features of TV
Foul-smelling, frothy, yellow-green, purulent discharge
Vulvovaginal pruritus
Burning sensation
Dyspareunia
Dysuria
Strawberry cervix (erythematous mucosa with petechiae)
How is TV diagnosed
Saline wet mount of vaginal smear: motile trophozoites with multiple flagella
If wet mount is inconclusive, perform culture.
pH of vaginal discharge > 4.5
