Endo Repro Koulton Flashcards
Fhs lh tsh hcg
Alpha subunit
Follicular phase
Onset menstration to preovulatory LH surge
Estradiol
Lumen
Tart with LH surge to start menstration
Theca
LH cholesterol to androstenedione and testosterone
Granulosa
FSH aromaiation a and t to estradiol
FHS LH
High follicular down luteeal from high progesterone
Corpus luteum to albicans
FSH up and estradiol positive feedback later LH surge
What day try and conceive
14
If cycle 114 days when have intercourse
Day 100…first half can be off but once ovulate bleed 14 days later ***
GnRH
Decapeptide from arcuate nucleus cause secretion of gonadotrops (LH and FSH)
LH FSH forms
Release and storage
As estradiol goes get get wht
Positive feedback and surge
Gonadotrops on GnRH
Decrease
Why get progesterone follicular
Prior to ovulation the unruptured luteinizing Graafian follicle begins to produce increasing amounts of progesterone
When secretion of progesterone by CL reaches max
5-7 days after ovulation and returns before menstration
Primordial follicles
Undergo sequential development, differentiation and maturation until mature
Rupture follicle
Release egg ovum
Luteinization of ruptured follicle
Makes cl
When do oocytes become surrounded by precursor granulosa cells
8-10 weeks
Called a primordial follicle
In ADULT ovary, graffiti follicle form
Inner most 3-4 layers of multiplying granulosa cells become cuboidal and adherent to the ovum thi is called cumulus oophorus
A fluid filled antrum forms among the granulosa cells
Antrum enlarges and the centrally located primary oocyte migrates t the wall of the follic;e
The innermost layer of the granulosa cells of the cumulus become elongated and for the corona radiata
Corona radiata
Released with the oocyte at ovulation
Innermost layer of granulosa cells of the cumulus becomes elongated and rorm it
LH surge
Ovulation
After ovulation
Granulosa undergoes luteinization
Corpus luteum
Lutenized granulosa cells, theca cells, capillaries and CT from corpus luteum
-make progesterone
Lifespan CL
9-10 days
Pregnancy not occur what is fate of CL
Gradually replaced by an avascular scar called corpus albicans
How does pituitary respond decreasing p and e
Increase LH and FSH
Diagnose menopause
FSH high from no neg feedback
2 zones of endometrium
Basalis and functionalis
Functionalis
Outer potion
Cyclic changes during menstrual cycle and sloughed off
Spiralis
Basalis
Remains relatively unchanged
Basal arteries
Provides stem cells
Cyclic changes
Menstrual phase
Proliferative
Secretory phase
Cycle day 1
1st day menstruation
When reach maximal thickness
Secretory phase
Proliferative 4-8 mm
Secretory 8-14. Ml
Conception not by day 23
CL regress, decrease p and e, endometrial involution
Menstration cycle
Terminal event of process for uterus to get baby
Intact coagulation pathways important
Healed with normal hemostasis
Need platelets and clotting factors
Warfarin
Heavy enstruation
Girls with HEAVY period at 12 years old. What have
Von williebrands disease.
Age menarche
12.43
2-3 years of thelarche at tanner IV
Primary amenorrhea
No menstration by 13 without secondary characteristics
By 15 with sex characteristics
Excessive flow
Greater than 80 cc (30 cc normal) associated with anemia
-changing pat q1-2 hours and considered excessive if >7 days
Puberty and factors
10-16
Geographic location, genetic, nutritional status
20 week in uteru
Have 6-7 million oocytes
HPO suppressed when
4-10 years
Function of low level gonadotropins and sx steroids during prepubertal period
Gonadostat sensitivity to the negative feedback of low circulating estradiol
Intrinsic central nervous system inhibiton of the hypothalmic GnRH secretion
8-11
Increase serum DHEA and DHEaS
Initial endocrine changes associated with puberty
Adrenal androgen production and differentiation by zone reticularis of the adrenal cortex
Rise in adrenal androgens
Growth of axillary and pubic hair
11
Loss of sensitivity by gonadostat to the negative feedback of sex steroids. In combination with the intrinsic loss of central nervous system inhibiton of GnRH
Sleep associated GnRH secretion occur and gradually shift into adult type secretory patterns
Increase GnRH 11
Promotes ovarian follicular maturation and sex steroid production, which leads to the development of secondary sex characteristics
Mid to late puberty
Positive feedback mechanism of estradiol on LH release from anterior pituitary is complete and osculatory cycles are established
Thelarche requires ___
Estrogen
Pubarche/adrenarche requires ___
Androgens
Maximal growth or peak height velocity when
2 years earlier in girls and 1 year before menses
Menarche
Require pulsatilla GnRH from hypothalamus, FHS< and LH from the pituitary, estrogen and progesterone from the ovaries, normal outflow tract
Thelarche race
African American and Hispanic go through before caucasion
Tanne 1
Preadolesence, elevate pilla
2
Breast bud
3
Enlarge breast aerola
4
Projection secondary mound
5
Projection papilla recession aerola
1
No pubes
2
Slight pigment and down
3
Coarser hair pubes
4
Adult hair not medial thighs
5
Medial thighs and inverted triangle
Precocious puberty
Secondary sexual characteristics prior to 2.5 SD expected
8 year old girl 9 boys
Rare
What do
Thorough evaluation to rule out serious disease and stop premature fusion of long bones so as adults short
Tall when prsent then close then short
Emotionally hard for girls and icnreased risk sexual abuse
Heterosexual precocious puberty
Dev of secondary sex characteristics opposite expect
Virilizing neoplasma
CAH
Exogenous androgen exposure
Isosexual precocious puberty
Premature sexual maturation that is appropriate for the phenotype of the affected individual
Constitutional and organic brain disease
-tumors, trauma, infectious process
Heterosexual precocity androgen secreting neoplasms
Rare
Usually in ovaries
Diagnosed PE and radiological exam and treated with surgical
CAH heterosexual
Most commonly 21 hydroxylase
Classical-birth of females with ambiguous genetalia-if untreated virilization and short
Nonclassical-resemble POCS premature pubarche
Isosexual precocity true
Arises from premature activation of the normal process of pubertal development involving the HPA
Isosexual precocity pseudosexual precocity
Exposure of estrogens independent of HPO axis
Estrogen producing tumors
Diagnose true
Idiopathic most common
Give GnRH see rise in LH
CNS disorder
-willl have neurological symptoms before sexual dev
MRI head
Treat true
Gnrh agonsit (leuprolide acetate) -decrease gonadotropins to prepubertal
Not treater true
Will not attain 5 foot adult height
Pseudo
Without activation of HPO
Ovarian tumor, exogenous estrogenic, mccune Albright and peutz=jeghers
Mccune Albright
Somatic mutation during embryogenesis which causes them to function independent of their normal stimulating hormones
5%
Multiple cystic bone defects, cafe au last spots
Adrenal hypercortisolism
Peutz jeghers
Associated with a sex cord tumor that secretes estrogen
GI polyposis and mucocutaneous pigmentation
Delayed puberty
Secondary sex not by 13 or thelarche not by 14
No menses 15 or 16
Menses not 5 years after thelarche
Cause
Hypergonadotropic hypogonasism
-turner/gonadal dysgenesis
FSH>30
Hypogonadotropic hypogonasism (FSH LH <10) Kallman, anorexia, pituitary tumors, hyperprolactinemia, drug use
Anatomic causes
-mullerian agenesis, imperforate hymen, transverse vaginal septum
Amenorrhea primary
No spontaneous uterine bleeding by 13 without secondary sex characteristics
No menstruation by 15 years with secondary sexual development
Amenorrhea secondary
Patient with prior menses has absent at least 6 months
If primary amenorrhea
Does she have secondary sex
Low-look FSH LH
Primary with absence of secondary sex
FSH LH<5
Hypogonadotropic hypogonadism
MRI
Causes hypogonadotropic hypogonadism
Lesions/tumors HPA Anorexia/exercise Hyperprolactinemia Kallman Constitutional delay -most common, hereditary factors may play role 20%
Most common delayed puberty
Constitutional
Hypogonadotropic hypogonadism kallman
Mutation KAL gene on X chromosome that prevents the migration of GnRH neurons into hypothalamus
Have anosmia or hyposmia
Hypergonadotropic hypogonadism (chromosomal or injury to ovaries by surgery, chemo, radiaiton
Ok
Treat to evaluate delayed puberty
MRI, FSH, karyotype, progesterone, prolactin
What is karyotype comes back with Y chromosome
Gonadectomy is recommended to prevent malignant neoplastic transformation
Primary amenorrhea with absence of secondary sexual characteristics
FSH>20 L LH >40
Hypergonadotropic hypogonadism
Karyotype to rule out Y chromosome
Cause hypergonadotropic hypogonadism
Gonadal agenesis/dysgenesis of the presence of an abnormally developed gonad due to chromosomal defects (TURNER 45 XO)
Turner
MOst common female gonadal dysgenesis
No signs of secondary sexual characteristics
Mosaicism in 25% may have normal phnenotype with spontaneous onset of puberty and menarche
Signs turner
Broad flat chest wide neck
Streak ovaries
No puberty
Coarctation aorta
Primary amenorrhea with secondary sexual characteristics US show no uterus
Do karyotype
Androgen insensitivity syndrome
46XY
Male levels of testosterone
Defect in androgen receptor
Testes in abdominal wall
-secrete antimullerian hormone so no uterus
-external female genetalia with no pubic hair
Breast development with small aerola/nipples
-caused by estrogen secretion in testes and conversion of androgens to estrogen int he liver
Mullerian dysgenesis/agenesis
Primary amenorrhea, normal breast dev, levels of testosterone with females
-mullerian defects that cause obstruction of vaginal canal
—imperforate hymen or a transverse septum
-absence of normal uterus is known as mullerian agenesis
-failure of Müllerian ducts to defuse distally and to form the upper GI tract will have a vaginal dimple
-absent uterus but may have a unilateral or bilateral rudimentary uterine tissue, tubes and ovaries
-associated with renal abnormalities
-IV pyelogram should be ordered to assess urinary system
Abnormal shaped uterus…
Order IV pyelogram to assess urinary system or CT to see ureters
Get IVP
Androgen insensitivity
Normal breasts no sexual hair
Normal looking female external genetalia
Absent uterus and upper vagina
Karyotype 46 XY
Male range T level
Test with gonadectomy
Mayer rokitansky kuster hauler
Normal secondary dev and external female genetalia Normal female range testosterone Absent uterus and upper vagina Normal ovaries 46 XX Renal abnormalities get IVP
Most common cause or primary amenorrhea in women with normal breast dev.
Primary amenorrhea with secondary with urterus : outflow obstruction
Normal uterus
Imperforate hymen or transverse vaginal septum
Imperforate hymen
Present complaining monthly dysmenorrhea without vaginal bleeding
Vaginal bulge and midline cystic mass
US confirm normal uterus
Do hymenectomy
Transverse vaginal septum
Simila symptoms but no vaginal bulge
Diagnosed with MRI
Correct with surgery
Secondary ameonrrhea
Absence for 6 months after having it
Causes secondary amenorrhea
Pregnancy! Get pregnancy test
What do if present with secondary amenorrhea
Look for weight change, preg test, exercise, diet, ill, abnormal facial hair, galactorrhea, dyspareunia, hot flashes or night sweats
Uring HcG, TSH prolactin, FSH
Secondary amenorrhea: hypothyroidism porlactinoma
Normal TSH
Galactorrhea is most common symptom of hyperprolactinemia
Really high >100
-MRI for empty sella, pituitary adenoma
High prolactin<100
-if MRI negative consider other causes
Secondary amenorrhea hypothyroidism
Normal prolactin
Abnormal TSH
Mild hypothyroidism-hypermenorrhea or oligomenorrhea,
Treat-restore menes
Abnormal micro vs macroadenomas
<10 mm on MRI-slow growing, manage , bromocriptine
> 1 cm-bromocriptine, resection or craniotomy
What causes prolactin <100
Ectopic production
Breast feeding and stimulation
Exercise
Head trauma
Hypothyroidism
Liver renal failure
Meds
Cause proacting >100
Pituitary adenoma
Empty sella
Secondary amenorrhea did tsh prolactin and negative
Progesterone challenge test
-give provers for several days then stop it. Positive bleed usually POCS
Negative-no bleeding-inadequate estrogen or abnormal outflow tract
Negative progesterone channelge
Estrogen/progesterone challenge
Negative-outflow tract of
Positive-abnormalities with HPA or ovaries
—-
Positive e/p test elevated fsh and lh
Hypergonadotropic hypogonasism
Ovarian abnormalities
Positive e/p test and normal or low FSH LH
Pituitary or hypothalmic abnormality
Get MRI
-no tumor then a hypothalmic cause of amenorrhea diagnosis
Anatomic causes
Asherman
Cervical stenosis
Asherman
Incomplete abortion but had normal periods
DNC was done…can be scarring so menstruation come out
As age sometimes opening of cervical os narrow
Secondary amenorrhea normogonadotropin hypogonadism
Adrenal disorders, ovarian, other
Adrenal nonclassical
CAH increase 17 hydroxyprogesterone
-no genital abnormalities
But have hirsutism, acne and menstrual irregular near puberty
Cushing
Central obesity, moon like faces, buffalo hump, HTN, striae, hirsutism, acne and irregular menses
High cortisol
Adrenal androgen secreting tumor
DHEAS>700
Ovarian disorders
POCS
Ovarian androgen secreting tumor
-sertoli leydig tumros (T>200)
Other
Exogenous androgens
POCS
10%
Leading cause of female anovulatory infertility
Insulin sensitivity
-decrease insulin hypersecrtion
Elevated insulin and androgen levels reduce the hepatic production of sex hormone binding globulins
-increased T
Diagnose POCS
Oligomenorrhea and amenorrhea
Biochemical or clincial signs or hyperandrogenism
-LH to FSH 2:1
US revealing multiple small cysts beneath the cortex of the ovary
Lab POCS
Increase LH decrease FHS
Extraglandular armoatization, chronic anovulation, decreased follicular maturation, stim of stroma and theca
Androgen excess
POCS stuck in ___ phase
Follicular
Increase stroma stimulation increase LH
Chronic anovulation
Features POCS
Anovulation T LH up Acyclic estrogen production Fat Acanthosis nigricans Lipid abnormalities DM CVD Anovulation -increase chance endometrial hyperplasia and cancer
Treat POSC
Weight loss
OC
-suppress FSH and LH
-allow regression of T and androstenedione of ovary
Estrogen stimulates the sex hormone binding globulin
Clomiphene citrate
-can induce ovulation
Ovarian diathermy/laser
Spironolactone and or electrolysis
-competes for testosterone binding sites thereby exerting. Direct antiandrogenic effect at target organ and also interferes with steroid enzymes and decreases testosterone production
Insulin sensitizing agents-biguanides (metformin)
Secondary amenorrhea hypergonadotropic hypogonadism
Pct neg, e p positive, check fsh lh
FSH>20 LH>04
-hypergonadotropic hypogonadism
Postmenopausal ovarian failure-average age of menopause is 51
Premature ovarian failure before 40
Cause-ovarian injury from surgery, pelvic radiation, chemo, carrier status of fragile syndrome, autoimmune, mumps
FSH LH<5
MIR for pituitary tumor
Normal=hypogonadotropic hypogonadism
-anorexia, bulimia
-chronic renal dinsuffiency< DM, IBD
Radiation, exercise, malnutrition, HPA destruction
History hyperandrogenism
PCOS and late onset CAH
Neoplastic disorders
PE-hirsutism, acne, alopecia document, cushing, acanthosis nigricans, bimanual exam for ovarian enlargement
Acanthosis nigricans
Dark velvety skin
Hirsutism
Excess terminal hair in male pattern baldness
Represents exposure of hair t androgen excess
Virilization
Masculinization of a females associated with marked increase in circulating T
Enlargement of clit, temporal balding, deep voice, decreased breast, loss sof female body fat distribution, and hirsutism
Fast rapid onset
Ferrima galloway scale
For hirsutism
Labs hyperandrogenism
17 hydroxyprog
24 hr urinary cortisol and overnight dexameth suppression test
Prolactin and tsh
Glucose and lipid
Testosterone and DHEA-S
(If DHEEAS over 7000 suspect adrenal androgen producing tumor and if T over 200 suspect ovarian androgen producing tumor)
Polymenorrhea
<21 days
Menorrhagia
Prolonged bleeding at normal intervals
Menorrhagia
Irregular episodes bleed
Menometorrhagia
Heavy and irregular
Intermenstrual bleeding
Scant bleeding at ovulation for 1 to 2 days
Oligomenorrhea
Menstrual cyclets occurring>35 days but less then 6 months
Dysfunctional uterine bleeding
Abnormal from HPA and bimodal first start and menopause
PALM-COEIN
Palp structural
Polyp, adenomyosis, leimyoma, malignancy
Coein
Coagulopathies, ovulation dysfunction, endometrial causes, iatrogenic, not yet classified
Coaguloapatheis
Heavy flow
Vw
Ovulation year dysfunction
POC
Endometrial causes
Infection
Iatrogenic
IUD, hormones
Lab test abnormal uterine bleeding
Pregnancy test no matter what
Cbc, Von Willie Randolph, pT PTT, TSH, chlamydia
Endometrial biopsy to look for endometrial hyperplasia and cancer
Treat massive bleeding
Hospital 2 large IV bores give IV conjugated estrogen then hormonal treatment
MIRENA! Within 2 years stop bleeding
Treat moderate bleeding
Combination OCP, mirena
Unresponsive to conservative therapy bleeding
D and C, polypectomy, myomectomy, endometrial ablation, hysterectomy
Ambiguous genitalia
Clitoromegaly
Clitoral agenesis
Bifid clit
Midline fusion of labiascrotal folds
Cloaca-no separation between vagin and bladder
What do if present with ambiguous genetalia
PE, US, hormonal studies, karyotype General
In general with suboptimal development of penile or scrotal structure the infant is usually assigned a female gender
Females pseudohermaphroditism
Masculinization in utero of femal fetus -CAH -ingestion of exogenous hormones -androgen secreting tumors of mother adrenal or ovaries (sertoli leydig) See clitoromegaly
Internal genital organs develop normally
Male pseudohermaphroditism
Commonly results from mosaicism and can occur with varying degrees of virilization and mullerian development
-androgen insensitivity syndrome
Androgen insensitivity
46XY testes undescended
Remove gonads risk of cancer
Occur mullerian inhibiting substance made lack of Müllerian duct development
X linked
Ambiguous genetalia
True hermaphroditism
Both male and female externally and internally
Labia agglutination
Treated by estrogen cream and massage to separate the labia majora
Fox ford he disease
Severe pruritis raised yellow retention cyst in axilla and labia majora and minora resulting form keratin plugged inflammation of apocrine glands
Inclusion cysts-most common genital cyst
Located beneath the epidermis and are mobile, nontender, spherical and slow growing. Usually no treatment
Develop when hair follicles become obstructed the deeper portion of the follicle swells to accommodate the desquamated cells
Vulvar varicosities
Can enlarge and become painful in pregnancy, have characteristic blue color
Lentils (freckles) and nevi (moles)
Need to distinguish from melanomas
Urethral caruncles
Small fleshy red outgrowth at distal edge of urethra
Kids caused by spontaneous prolapse of the urethral epithelium
Post menopausal women is secondary to contraction of the hypoestrogenic vaginal epithelium resulting in everting of the urethral epithelium
Vulvar vestibulitis*
Rare condition in whihc one or more of the minor vestibular glands becomes infected
Bright red super tender
1-4 mm erythematous dots that are extremely tender
Characterized by severe introital dyspareunia and occasionally vulvar panin
Can try topical estrogens/hydrocortisone or surgical therapy may be required
Sebaceous cyst
Caused by inflammatory blockage of sebaceous gland ducts
Small smooth nodular masses usually on inner surface of labia minora and majora
Contain a cheesy sebaceous material
Fibroams
Most common benign solid tumors of the vulva
Slow growing, most range from 1-10 cm
Can become gigantic (250 lbs)
Lipoma
Slow growing tumros composed of adipose cells
Hide adenoma
Rare lesion arising from sweat gland of the vulva
Syringomyelia
Eccrine gland tumor
Neurofibroma
From Von recklinghausen disease
Angiomatosis
Appear as multiple 2-3 mm red lesions usually in 4th and 5th decade
Most common benign solid tumros of vulva
Fibroma
Vulvar vestibulitis
Painful insertion , punctuated lesions at entrance when tough with q tip super painful
Bartholin gland
5 and 7 o clock position
Vulvar hematoma
Collections of blood that collect following trauma
Bike risde
Close observation and occasional surgery
Female genital circumcision
More common in africa and Eastern Asia
Degree of anatomic change has an effect on infection risk, sexual function and vaginal delivery
Obstetric related trauma
Usually from lacerations or episiotomies can result in scarring
Atrophic vaginitis
Loss of estrogen (menopause, surgery)
Atrophy of external genetalia
Minora regresses and majora shrinks
Loss of vaginal rugae
Vaginal introitus constriction
Treat atrophic vaginitis
Topical estrogen
Oral estrogen to prevent reoccurrence
Lichen simplex chronicus
Local thickening of epithelium that result from prolonged itch scratch cycle
Pruritis
Exam liche simplex chronicus
White reddish thickened leathery, raised surface
Looks similar to psoriasis
Biopsy-elongated retention ridges
Hyperkeratosis of the keratin layer
Treat lichen simplex chronicus
Moderate strength steroid ointments with antipruritic agents
Lichen sclerosis-most common menopausal
Can cause genital structural
Can get squamous cell carcinoma
Itching, pruritis, dyspareunia
Parchment papare onion scaling,
Thin epithelium loss or rete ridges and inflammatory cells lining b***how tell apart
Clobetasol
Lichen sclerosis
Loss of labia minora
Lich simplex vs sclerosis
Sclerosis-hyaline zone in the superficial dermis from edema
Both hyperkeratosis, but epidermis thinner in sclerosis
Acanthosis with elongated rete ridges simplex
Lichen plants
Purplish polygonal papules that may appear in an erosive form
Vulvar vaginal gingival syndrome
-when lichen planus involves the vulva, vagina, and mouth
Symptoms-vulvar burning, severe insertional dyspareunia
Treat-topical and systemic steroids
Psoriasis
AD
Velvety but may lack the silver scaly patches
Eczema
More erythematous presentation
Pemphigus
Autoimmune blistering disease involving the vulvovaginal and conjunctival areas
Bechet syndrome
Classically involves ulcerations int he genital oral areas with uveitis
Crohn
GI but vulvar ulcerations can occur due to fistulization
Aphthous ulcers
Superficial and painful and are more common in mouth
Decubitus ulcer
When chronic pressure is applied or secondary to tissue being moist secondary to urinary incontinence
Acanthosis nigricans
Most commonly found in the intertriginous area, vulva, axilla or nape of the neck
Appear as a demarcated brown pigmented thickened are int he superficial layers of the skin
Is mot commonly related to insulin resistance and obesity but can be linked to other benign conditions and malignancy
Contact dermatitis
A careful history may identify the specific irritant
PE may reveal erythema, edema, excoriation or ulceration
May need biopsy
Imperforate hymen
After birth a bulging membrane like structuremay be noticed into e vaginal opening can block mucus
If not detected until menarche see thin dark blue with old menstrual fluid
Vaginal transverse septum
In upper and middle thirds of vagina often a small sinus tract or perforation will be present whihc allows the egress of menstrual flow
May only become apparent when intercourse is impeded
Midline longitudinal
Created a double vagina, a longitudinal septum can attach to the lateral wall thus creating a blind vaginal pouch
These septa are usually associated with various duplication anomalies of the uterine fundus
Vaginal agenesis
Absence except most distal portion from urogenital sinus
Rokintansky kuster hauler if uterus is absent but Fallopian tubes are spread
Adenosis
Islands of columnar cells in normal squamous epithelium
DES
Gardner’s duct cyst
Arise from the remnant of the wolffian duct
Vary in size from 1-5 cm and are found int he lateral walls of the vagina
Asymptomatic mostly and no intervention
Urethral diverticula
.3-3 cm sac like projection in anterior vagina alons posterior urethral
UTI, dysuria, urinalysis leak,
Give urethral dilation or excision
Inclusion cyst
From infolding of vaginalis epithelium
In posterior or lateral wall in lower third of the vagina
Frequently associate with gynecological surgery or lacerations from childbirth
Endometriosis
Implants can be seen inv agina and change in appearance with menstrual cycle
Bartholin cyst-most common vulva vaginal tumor
3 cm asymptomatic
Unilateral
Need to biopsy in women 40+ to rule out bartholin carcinoma
Bartholin gland abscess
From blockage and accumulation of purulent material and is painful
Treat-word catheterization
Leave in 4-6 weeks which promotes an epitheliazed tract for drainage of glandular secretions
OR
Marsupilization
-creates a new ductal opening by everting the cyst wall onto the epithelial surface where it is sutured with interrupted absorbable sutures
Most common cause of a final trauma
Sexual assault
Dermatological atrophy
After menopause the vaginal rugations flattern out and the vaginal epithelium becomes thin, pale and inelastic
Vaginal pH rises
Vulvar neoplasms mostcommon
Squamous cell carcinoma
Who tests squamous cell carcinoma of vulva
Post menopausal
Long history of scratching
Melanomas, adenocarcinomas, basal cell carcinoma, sarcoma
VIN III
In situ linked to vulvar cancer and VIN I II III based on depth of epithelial involvment
VIN III
High grade
VIN usual
HOV 16 smoking and immunocompromised
Gardasil
Differented VIN
Not HPV
Vulvar dermatological like lichen sclerosis
Clincial VIN III
Pruritus is most common
No absolute diagnostic appearance
-most elevated, but color can be white, red, pink, grey or brown
20% of lesions have a warty appearance
VIN III diagnosis
Inspection of vulva and biopsy
Manage VIN III
Excision
Skinning vulvectomy removes skin is rarely required
Laser therapy is useful if lot around clit or bottom
Paget
Rare
Postmenopausal white females
Itching, tenderness are common
Well demarcated and eczematois appearance and white plaque like lesion
Biopsy paget cells
Superficial excision to clear
Squamous cell carcinoma clincial
Post menopausal
Vulvar limo
Present with a lesion that is pruiritis, raised, ulcerated, pigmented or warty on labia majora
Requires biopsy
Method of squamous cell carcinoma spreas
Direct extension to adjacent structures
Lymphatic embolization to regional lymph nodes
Hematogenous to distant sites (lung, liver, bone)
Manage SCC
Radical vulvetomy and regional lymphadenectomy
Wide local excision with inguinal lymph node , if positive nodes also get chemo
Malignant melanoma
Second most common vulvar
Postmenopausal white women lesions noted on labia
Wide local excision
30% comparable
Verrucous carcinoma
Warty cauliflower confused with condyloma
Variant SCCC
Don’t radiate may induce anaplastic transformation
Bartholin gland carcinoma
Bartholin gland prob after 40
Painless
No history
Recurrence common
Basal cell carcinoam
Appear as a rolled edge ulceration
Do not metastasize
Wide local excision is adequate
Preinvasive disease of vagina etiology
HPV
50-90% with VAIN have prior neoplasia or cancer of cervic of vulva
Diagnose VAIN
Asymptomatic
Considered with an abnormal pap in a woman who is status post hysterectomy or has no demonstratable cervical lesion
Colposcopic directed vaginal biopsy
Manage VAIN
If lesion involves the vault
-surgical excision to treat and exclude vaginal cancer
Multifocal-treat with laser therapy or topical 5-FU if unsuccessful ay require vaginectomy
Carcinoma vagina
Rare, 60 (most common SCC)
Abnormal discharge, bleeding, urine blood
Exophytic or ulcerative
-direct to bladder urethra rectum, or lateral
Lymphatic spreas
Hematogenous spread
Diagnose with punch biopsy
Diagnose carcinoma vagina
Punch biopsy
Treat carcinoma vagina
Radiation chemo
If lower 1/3 groin nodes removed
Upper vagina-surgery radical hysterectomy, upper vaginectomy bl lymphadenectomy
Prognosis carcinoma of vagina
5- year survival rate for squamous cell vaginal cancer is 50%
Adenocarcinoma
Metastatic from cervix, endometrium or ovary
Clear cell carcinoma from DES
RADICAL HYSTERECTOMY and vaginectomy or radiation
Malignant melanoma
55 distal anterior wall
Poor prognosis
Sarcoma Botryoides
Presents as a mass of grape like polyps protruding from the introitus
Histological the tumor is embryonal rhabodomyosarcoma
Mean age is 2-3 years old
Treat-surgical resection, chemo, radiation
Normal vagina
Nonkeratinized stratified squamous epithelium
Acidic vagina
Lactic acid and hydrogen peroxide producing lactobacilli
-protect sti
Increase alter microflora
Antibiotics
Douching
Intercourse
Foreign body
Nitrosine paper
Acidic yellow
Basic green or blue
Vaginal discharge do nitrazine paper
Posterior fornix beneath cervix and put under microscope
Bacterial vaginosis
Most common vaginitis
-gardnerella vaginalis most common
Risk BV
New or multiple sex partners, smoking IUD, douching
Symptoms BV
Asymptomatic milky discharge fishy amine odor after intercourse
Diagnose BV
Saline wet mount clue cells
KOH whiff test
PH>4.5
Treat BV
Metronidazole
DONT TREAT partner not std
Vulvovaginal candida
Second most common
Candia
Risk candida
Increase estrogen
DM, antibiotic, steroid
Symptoms candida
Pruiritis, irritation/dyspareunia
Clumpy cottage cheese
Diagnose candida
10% KOH wet prep positive for budding yeast
Pseudohyphae
<4.5 pH
Treat candida
Diflucan
Miconazole
Trich
T vaginalis flagellated protozoan
Strawberry cervix
Symptoms trich
Asymptomatic
Dyspareunia , vulvovaginal irritation, occasional dysuria
Green yellow frothy discharge
Diagnose trich
Saline wet mount motil trichomonads pH>4.5, strawberry cervic
Treat trich
Metronidazole
Test partner
Benign conditions of the uterus, cervic, ovary and Fallopian tubes
Ok
Absence Y chromosome absence mullerian inhibiting substance
Development of paramesonephric system with the regression of mesonephric
Describe paramesonephric duct
Arise 6 weeks gestation and by 9 weeks they fuse in the midline to form the uterovaginal primordium
Later the septum resolves between he fused paramesonephric ducts leading to the development of a single cervix and uterus
Uterus didelphysis
Failure of the paramesonephric duct to fuse can lead to
-uterus didelphysis-2 separate uterine bodies with its own cervic, attached Fallopian tube and vagina
Bicornuate uterus
Rudimentary horn
Birnuate uterus
With or without double cervices
Incomplete dissolution of midline fusion fo paramesonephric ducts
Septate uterus
Failure of formation of Müllerian ducts
Unicornate uterus
Mullerian agenesis (Meyer rokitansky kuster hauler syndrome)
The complete lack of development of the paramesonephric system
-absence of the uterus and msot of the vagina
Most common congenital anomalies of cervic
Malfusion of paramesonephric ducts
Didelphys cervix and septate cervix
Unicornate uterus
Check for renal abnormalities
Majority of uterine and cervical anomalies
Spontaneous
DES
-small t shaped endometrial cavity
Cervical collar deformity
Fibroid leiomyoma
Smooth msucle (polyp is glandular tissue)
Most common
Higher age more incidence
Rarely malignant
Familial
Symptomatic fibroids
Excessive uterine bleeding , pelvic pressure, pelvic pain and infertility
Most common indication for hysterectomy
Fibroids
Risk factors fibroids
Increasing age
African america
Nulliparity
Family history
Fibroids pathogenesis
Hormone, e and p stimulate it
Treat fibroids
Block or change hormones
Preg and fibroids
They enlarge
Characteristics fibroids
Spherical whirled appearance can degenerate and cause pain
After menopause fibroid
Shrink and go away
Subserosal fibroid
Beneath uterin serosal surface
Can attach to blood supply of the omentum or bowel mesentery an lose uterine connection thus becoming parasitic fibroid
Intramural fibroid
Fibroid arises within myometrium
Most common *
Submucosal fibroid
Beneath endometrium
Can be pedunculated and come through the cervical os
Prolonged or heavy menstrual bleeding is common
Cervical and intraligamentous fibroids
Arise between broad ligaments
Symptoms fibroid
80% uterine asymptomatic
Pelvic lower back pain
Pelvic pressure fullness
INFERTILICY if submucosa
Frequency urination
Signs bimanual exam fibroid
Enlarged, irregularly shaped uterus
If palpated mass moves with the cervic it is suggestive of a fibroid uterus
The degree of enlargement is described in week size used to estimate equilvent gestation size
US fibroid
Performed and can help distinguish between adnexal masses and lateral leiomyoma
Differential for fibroid
Ovarian neoplasm
Inflammatory mass
Pelvic kidney
Bowel mass
Colon cancer
IMAGINGG
Treat fibroid
E and p ocp
-1st idea
Progesterone only
-depo, minera
GnRH agonist
-depo-Lipton
-can decrease size in 3 months
Usually used to alter route of surgery
Surgery fibroma
Myomectomy
Endometrial ablation
Uterine artery embolization
Hysterectomy
-definitive harpy
Myomectomy
Future deliveries must b c section
Often grow back
Endometrial polyps
From endometrium create soft friable protrusion into endometrial cavity
Glandular
Symptoms endometrial polyps
Menorrhagia, spontaneous or post menopausal bleeding
Diagnose polyp
US endometrial stroke
-saline hysterosonography and hysteroscopy allow better detection
Benign or malignant polyp
Benign hyperplastic mass
Why remove endometrial polyp
Endometrial hyperplasia and carcinoma may also present as polyps
Nabothian cervical cyst
Normal variant
Opaque with a yellow or blue hue
3cm 3 mm
From squamous metaplasia in which a layer os superficial squamous epithelial cells entrap a layer of columnar cells beneath its surface
-columnar cells continue to secrete mucus and a mucus retention cyst is formed
Cervical polyp
Ectocervical and endocervical polyps are most common benign growths on the cervix
Symptom cervical polyp
Non coital bleeding or menorrhagia
Treat cervical polyp
Remove in office benign
Endocervical polyp
More common
Beefy red in color
Arise from endocervical canal
Ectocervical polyps
Less common
Pale in appearance
Endometrial hyperplasia
Thickened endometrium from estrogen
Who get endometrial hyperplasia
PCOS and anovulation
Granulosa heca cell tumors-estrogen producing tumors
Obese-secondary to peripheral conversion of androgens to estrogens in adipose cells
Exogenous estrogens-without progesterone
Tamoxifen
Endometrial hyperplasia is a precursor to endometrial cancer
2-3% of women will develop endometrial cancer
Simple hyperplasia without atypia
1% progress to cancer
Complex hyperplasia without atypia
3% progress to cancer
Simple hyperplasia with atypia
9% progress
Complex hyperplasia with atypia
27% progress
Symptoms endometrial hyperplasia
Intermenstrual , heavy or prolonged bleeding that is unexplained
Diagnosis endometrial hyperplasia
Sample the endometrium
US reveals endometrial lining >4 mm in postmenopausal female
NEED TO SAMPLE ENDOMETIUM
Treat endometrial hyperplasia
Simple and ocomplex without atypia give progestin and reasmple in 3 months
Simple and complex with atypia give hysterectomy
Turner
45XO abnormal gonad development
Small rudimentary streaked ovaries
Develop secondary sexual haracteristics but enter menopause shortly after
Complete androgen insensitivity syndrome /testicular feminization
46 Xa
Lack androgen receptors
Phenotypically female
Gonads need to remove after puberty bc of malignant potential
Fallopian tube anomalies
Rare
DES short distorted or clubbed tubes
Functional cyst ovary
Follicular, lutein, hemorrhagic, polycystic
Benign neoplastic cyst ovary
Epithelial-serous or mucinous cystadenoma
Sex cord-fibromas, granulosa theca cell, sertoli
Germ cell-mature cystic teratoma/dermis
Follicular cyst
Happen every month
Lined by one or more layers of granulosa cells
Develops when an ovarian follicle fails to rupture
Is CLINCIALLY significant if it gets large enough to cause pain
Corpus luteum cyst
May develop if the CL becomes cystic, larger than 3 cm and fails to regress normally after 14 days
Hemorrhagic cysts
More likely to cause symptoms
Caused by hemorrhage in CL cyst 2-3 days after ovulation
Polycystic ovaries
Enlarged ovaries with multiple simple follicles
Functional ovarian cyst
Theca lutein cyst!!
B/l large
Who gets theca lutein cyst
High serum levels of human hCG
Pregnancy, choriocarcinoma, hydatiform molar preg, ovulation induction (gonadotropins or clomic)
Theca lutein cysts regress when what
Gonadotropins levels fall
Functional ovarian cyst LUTEOMA OF PREGNANCY
Hyperplastic reaction of the ovarian theca cells
-secondary to prolonged hCG stimulation during pregnancy
Appear as reddish brown nodules
Surgical resection is not indicated
-usually regress spontaneously postpartum
When do luteoma of pregnancy regress
Post partum
When gonadotropin fall dont do surgery
PCOS functional ovarian cyst
Anovulation, hyperandrogenism, insulin resistance
Enlarged ovaries with multiple small follicles that are inactive and arrested int he mid antral stage
Increased LH levels promote androgen secretion from the ovarian theca cells, leading to elevated levels of ovarian derived androstenedione and testosterone
US POCS
String of pearls
Clincial features functional cyst
With every cycle
Asymptomatic
Regress during subsequent cycle
Large and can cause torsion
Diagnose functional cyst
Bimanual exam reveals and enlarged, mobile, unilateral cyst
US
Manage functional ovarian cyst
Asymptomatic and premenopausal-ocp
Symptomatic and pre menopausal-have to rule out ectopic, torsion, tubo ovarian abscess
Benign neoplastic tumros
Epithelial, sex cord, germ cell
Epithelial benign neoplastic ovarian tumros
Most common
Serous, mucinous, Brennan
Sex cord tumors
Fibroma, granulosa theca, sertoli leydig
Germ cell
Dermoid
-single most common benign ovarian neoplasm in a premenopausal female
Epithelial ovarian neoplasm
Derive from mesothelial cells lining peritoneal cavity and lining from surface of ovary
Mucinous, serous, endometrioid
Serous cystadenoma MOST COMMON EPITHELIAL OARIAN TUMOR
Surgical
Histology serous cystadenoma: the most common epithelial ovarian tumor
Psammoma bodies
-are more common in malignant serous cystadenocarcinomas
Mucinous cystadenoma
Large
Second ost common
Associated with a mucocele of the appendix
Rarely can lead to pseudomyxoma peritonei
-numerous benign implants are seeded onto the surface of the bowel and other peritoneal surface producing mucus
Remove appendix with mucinous
Ok
Serous vs mucinous
Smooth serous mucinous lumpy
Brenner tumor
Small smooth solid ovarian neoplasm
Benign
Large fibrotic component that encases epithelioid cells that resemble transitional cells of the bladder
33% of cases are associate with mucinous epithelial elements
Sex cord
Granulomas a theca, sertoli leydig, fibroma
If ultimate differentiation of cell types in tumors is feminine
Tumor is feminine
-a granulosa or theca cell tumor or often a mixed granulosa theca cell tumor (inhibin marker)
If cell takes on masculine differentiation
Sertoli leydig tumor
Granulosa
Any age
Estrogenic component
Low malignant
-precocious menarche and thelarche
Premenarchal uterine bleeding during infancy and childhood
Menorrhagia, endometrial hyperplasia and endometrial cancer
Breast tenderness, fluid retention, postmenopausal bleeding
Sertoli leydig
Less frequent
Makes androgenic
Hirsutism, temporal baldness, deep voice, clitoromegaly, defeminizing of the female body habitus to a muscular build
Virilizing vs hirsutism
Hirsutism-hair growth acne
Virilization-deep voice clitoral change, balding , androgenic body habitus
Fibroma
Most common benign solid ovarian tumor!!!!
Not secrete steroids
Meigs syndrome
Meigs syndrome from fibroma
Ascites and right pleural effusion in associationwith an ovarian fibroma
Flow of ascitic fluid through the transdiaphragmatic lymphatics into the right pleural cavity leads to meigs syndrome
Germ cell tumors
Younger
Cystic teratomamost common ovarian neoplasm in women of all ages!!!!!!
Benign cystic teratoma (dermoid)
30 yo
Kids-1/2 benign ovarian tumors
Bl
Slow growing <10 cm
Describe a dermoid
May contain differentiated tissue from all three embryonic germ layers (ectoderm, mesoderm, endoderm)
Mainly ectodermal-skin, sweat, sebaceous gland, hair follicles
Most teratomas benign or malignant
Benign
Cystic teratoma
Multicystic mass
Hair, teeth, mixed into sebaceous thick material
Rokintanskys protuberance
Rokintanjsy protuberance
Solid prominence located at the junction between the teratoma and normal ovarian tissue
Rupture cystic teratoma
Chemical peritonitis
Clincial features benign ovarian tumors
Nonspecific and asymptomatic
Enlarge slowly
Pain mild
Can be painful
Why would a benign ovarian tumor be painful
Twist on its pedicure (torsion)
Rupture of cyst resulting in pain and peritoneal irritation
-rupture can occur spontaneously with trauma, during a bimanual exam or with intercourse
Rupture with serous fluid may evoke little pain
Dermoid or mucinous rupture can be more irritating to peritoneum
Diagnosis benign ovarian tumors
Abdominal and bimanual pelvic exam
US
- simple vs complex
- dermoid cyst (tooth like calcification)
Tumor markers
CA 125 in post menopausal
Laparoscopy
- uterine fibroids, ovarian tumor and hydrosalpinx differentiation
- laparotomy is preferable to laparoscopy unless the mass can be removed without rupture
Manage ovarian neoplasm
Need to prove by surgical exploration and pathological exam!!!
If surgery need to collect pelvic washings for cytologic exam
-obtain frozen section for histological diagnosis
Definitive tratment depends on patients age and desire for future pregnancies
Manage epithelial ovarian tumros
Unilateral salpingo-oophorectomy
If mucinous cystadenoma tumor is diagnosed
—perform an appendectomy secondary to possible coexistence of an appendices mucocele
In young may do cystectomy for ovarian preservation
In older a total abdominal hysterectomy with bl salpingo oophorectomy is appropriate
Stromal cell tumor treat
Unilateral salpingo-oophorectomy when future pregnancies are a consideration
Fibroma treat
Even with meigs syndrome almost always benign
Remove ovary or treat by resection of the ovary in a young woman who desires a future family
Treat germ cell dermoid
Ovarian cystectomy
Carefully evaluate other ovary since they are bl in approximately 15-20%
Rare recurrence after surgical resection
Copiously irrigate pelvis to avoid chemical peritonitis
Fallopian tubes
Most benign and infectious or inflammatory
Malignant rare
Hydrosalpinx
Fluid filled tubes from previous infection
Pyosalpinx
Purulent filled tube from active infection
Malignancy fallopian
Some serous ovarian cancers may arise from Fallopian tube
Ovarian tosrion presntation
Acute onset of unilateral pain
Nausea and vomiting
Diagnose ovarian tosrion
US first line
Definitive by direct visualization
Treat ovarian torsion
Detorsion and ovarian conservation with an ovarian cystectomy
Salpingo-oophorectomy is performed if ovary is necrotic or you suspect malignancy
