female uworld Flashcards
PID causes (bacterias)
N. gonorrhea
C. trachomatis
Pelvic inflammatory disease
TX?
complications ? (IF DID NOT RECEIVE FULL TX TOO)
tx: MUST COVER BOTH ORGANISMS SO :
A- 3rd generation cephalosporin (CEFTRIAXONE, etc,…)
for gonococcal infection
PLUS always!
B- azithromycin or doxycycline
for chlamydia -not sensitive to b lactams
complication: INFERTILITY !!! (DUE TO FALLOPIAN TUBE SCARRING) tuboovarian abscess extopic pregnancy perihepatitis
Fitz-Hugh-Curtis syndrome
PID inflammation in the peritoneal cavity !!!!
Fitz-Hugh-Curtis syndrome is a rare disorder that happens when pelvic inflammatory disease (PID) causes swelling of the tissue around the liver. You may also hear it called “gonococcal perihepatitis” or “perihepatitis syndrome.” Pelvic inflammatory disease is an infection of a woman’s reproductive organs.
most common cause of tubal factor infertility
PID
fever
(lower) abdominal pain
mucopurulent cervical discharge
PID
low sperm volume and acidic pH of an ejaculate sample means
congenital absence of the vas deferens
is oral contraceptive use associated with OVARIAN FAILURE ?
if not, what is associated?
NO !!
-smokers or
- receiving radiation or chemotherapy
is related to premature ovarian failure (i.e. primary ovarian insufficiency
what is the role of oestrogen and progestin in oral contraceptive pills?
FUN FACT: if used as prescribed: reliable and reversible :)
OESTROGEN:
-prevents pregnancy by suppressing the midcycle gonadotropin surge, thereby inhibiting ovulation
PROGESTERONE:
- counteract the increased risk of endometrial cancer associated with unopposed effect of oestrogen
- enhance the contraceptive efficacy by decreasing the permeability of the cervical mucus to sperm
side effects of oral contraceptive pills
- breakthrough menstrual bleeding
- breast tenderness
- weight gain
rare: - DVT
- PE
- ischemic stroke
- MI (INCREASED IN SMOKERS AND PT OVER THE AGE OF 35 !!!!!!!!) esp. more than 15 cig per day
does past pregnancy or childbearing status affect OCP side effect?
NOOOOOO
is OCP contraindicated with DM?
if adequately controlled (WITH NO CV RISK) it is not.
Note: 1st generation (high dose oestrogen) can induce insulin resistance and cause glucose intolerance (compared to 2nd and 3rd generation)
effect of HDL and LDL levels with OCP use. what are the contraindicated?
low HDL:
- known CV risk
- no data to increased risk with ocp
so we LOOK at LDL high LDL (above 160 mg/dl): is contraindicated
ABSOLUTE CONTRAINDICATIONS TO THE USE OF OCP are: (6)
1- prior hx of thromboembolic event or stroke
2- hx of an estrogen dependent tumor
3-women over 35 WHO SMOKE HEAVILY
4- hypertriglyceridemia
5-decompensated or aactive liver dx (would impair steroid metabolism)
6- pregnancy
what is “COMPLETE” molar pregnancy ?
form of gestational trophoblastic dx (complete vs partial)
1- complete mole
HAS NO FETAL STRUCTURES (composed of entirely large edematous disordered chorionic villi that appear grossly as clusters of vesicular structures - “bunch of grapes”
—>
presents wit pelvic pain and vaginal bleeding,
uterus is much larger than the gestational age, b-HCG is HIGHHH d/t trophoblastic hyperplasia ,
ultrasound: central heterogenous mass with multiple cystic areas “swiss cheese: or “snowstorm” pattern
risk factors of molar pregnancies
1- extremes of maternal age
2- prior molar pregnancy
3- prior miscarriage
4- infertility
most common type of complete mole (molar preganncy) — 90%?
and whats less likely?
OVUM (has no maternal chromosomes d/t absence or inactivation) by one sperm.
chromosomes from the haploid 23 X chromosomes are duplicated forming: DIPLOID 46, XX (most common!!!) that contains only paternal DNA.
less likely: 2 sperms fertilize an empty ovum and create:
46, XY or 46, XX is possible too
what is the most common sex xhromosome abnormality in females?
47, XXX (incidentally found)
what is 47, XXY karyotype means?
Klinefelter syndrome
associated with hypogonadism in males
what causes klinefelter syndrome? 47, XXY
non disjunction of the sex chromosomes during meiotic division of the gamete of wither parent
what are partial molar pregnancies?
69, XXX OR 69, XXY
fertilization of an ovum with 2 sperms
- it contains fetal tissue and normal placental villi intermixed with hydropic villi
postpartum hemorrhage cause
failure of the uterus to contract and compress the placental site blood vessels. leading to uterine atony!!!
postpartum hemorrhage risk factors
1- prolonged labour
2- twin gestation
tx of postpartum hemorrhage
1- uterine massage
2- uterotonic medications (oxytocin)
3- fails—> surgery
what is the main supply of the pelvic organs? and uterus?
internal illiac arteries (hypogastric arteries)
branches to give uterine arteries
postpartum hemorrhage surgery goal
BILATERAL LIGATION of the internal iliac arteries (to stop uterine blood flow) so preventing the need for hysterectomy.
IMP NOTE: organs supplied by internal iliac arteries have collateral circulation
ANATOMY REVIEW BF
AORTA —> rt + lt common illiac arteries —>
1- internal iliac arteries—> uterine artery + internal pudendal artery ( anterior trunk —> runs through the sciatic foramina to supply blood to the perineum.
2- external iliac arteries —> femoral artery
what happens if an injury to the pudendal artery happens during vaginal delievery ?
vulvar hematoma
Heavy prolonge menses pelvic pain constipation urinary frequency enlarged irregular uterus obsetric complications
uterine leiomyomas
FIBROIDS
what are uterine fibroids
BEINIGN
monoclonal SM tumors (that develop within the myometrium)
major risk for fibroids
RACE
african american women 2-3 times more likely than caucasian women to develop fibroids (onset mid to late 20)
-early menarche is another RF
is there a correlation between ovarian ca family hx and fibroids
NO
remember ca: large immobile ovaries
what cancer u can get if u work in a textile factory ?
BLADDER CANCER (EXPOSURE TO CARCINOGENS)
symptoms:
- increased urinary frequency
- concomitant hematuria
progestin-only pill and fibroids relation ?!
used in symptomatic fibroids to decrease their size :)
prior deliveries increases the risk of what ? (increased parity)
1- adenomyosis
-pelvic pressure
-symmetrical enlarged tender globular uterus
2- endometrial tissue with the myometrium
3- DECREASED RISK OF FIBROIDS
red meat consumption increases risk of uterine ————?
fibroids
pts with symptomatic uterine fibroids are often treated ——
surgically with a hysterectomy
how does a fibroid appear grossly?
discrete, yellow-gray tumors !!
with a think pseudocapsule that separates the fibroid from the normal uterine myometrium
why fibroids lead to HEAVY MENSES???
because they increase the endometrial surface area (d/t mass effect) :)
how do we confirm fibroids (uterine leiomyoma) diagnosis?
confirmed with MICROSCOPY
reveals monoclonal proliferation of myocytes and fibroblasts !!
how do we confirm fibroids (uterine leiomyoma) diagnosis?
confirmed with MICROSCOPY
reveals monoclonal proliferation of myocytes and fibroblasts !!
because each fibroid arises from a single progenitor SM cell.
how does cervical ca present?
asymptomatic or
irregular, postcoital spotting (NOT HEAVY MENSES!!!)
where is cervical ca typically found?
in the cervical transformation zone
how does cervical ca look under microscope ?
dysplastic squamocolumnar cells with areas of atypia
how does endometriosis typically present? what is it
-painful menses (dysmenorrhea)
—> endometrial tissue implants outside the uterus!! rather than intrauterine mass (i.e in fibroids)
how is endometriosis seen microscopically
ectopic endometrial glands!! and hemosiderin-laden macrophages
how does pts with endometrial hyperplasia or cancer typically present?
-irregular, heavy menses
-thickened endometrium
(in fibroids its a mass in the myometrium)
histopathology of endometrial hyperplasia or cancer:
hyperplastic proliferation of irregular endometrial glands
microscopy of ovarian cancer>?
infiltration of the stroma by high-grade serous carcinoma.
note ovarian ca causes an adnexal mass!! rather than a solitary intrauterine mass(in fibroid)
describe peau d’orange rash
generalized, erythematous!!, may be tender or itchy.
skin texture: firm! and coarsely pitted! like an orange peel
inflammatory breast cancer !!!
PEAU D’ORANGE (w/ or w/o breast mass) and BREAST EDEMA!!
DVT causes
occurs due to hypercoagulability related to malignancy, surgery, or IV catheter placement
Can DVT affect upper extremities
yes, it presents with oedema and pain in the affected lamp
What happens if silicone breast implant ruptures
Lead to a foreign body reaction with local inflammation (e.g oedema, induration), And granuloma formation can result in a palpable, tender mess.
What are the two non-invasive breast cancers and the three invasive breast cancer?
Non-invasive: DCIS and Paget disease
Invasive: ductal carcinoma and lobular carcinoma and inflammatory breast cancer
characteristics laterrrr!!!!!
What are the two non-invasive breast cancers and the three invasive breast cancer?
Non-invasive: DCIS and Padget disease
Invasive: ductal carcinoma and lobular carcinoma and inflammatory breast cancer
Key features of DCIS (3)
- central necrosis
- precancerous lesion
- confined to ducts and lobules
Key features of paget disease (2)
- eczematous nipple lesion
2. extension of DCIS into ducts
Key characteristics of ductal carcinoma (2)
- most common type
2. nests and cords of cells
Key characteristics of lobular carcinoma (2)
- Small cells in single file
2. Mammary stroma invasion
Key characteristics of inflammatory breast cancer (2)
- peau d’orange
2. Dermal lymphatic invasion
Mastitis
Most common in ——
presents …
most commonly occurs in lactating women.
Presents with pain, breast swelling, erythema.
Most patients also have systemic findings such as fever, malaise and leucocytosis.
Two types of surgical incision scars
- Hypertrophic scar: thick, raised, and pink fibrous tissue line that FOLLOW the original incision.
- Keloid scars: occurs due to disorganised collagen deposits. thick, rubbery appearance and extend outside the incision borders
How can Turner’s syndrome (45, XO) patient get pregnant/method?
After checking renal cardiac and thyroid examinations.
IVF
notes:
Most women are infertile secondary to ovarian failure.
With sufficient oestrogen and progesterone supplementation, these woman can develop a thick endometrial lining that is substantial enough to support a pregnancy.
ovum from a donor!!! (60%)
How to restore fertility in women with hyperprolactinaemia
Bromocriptine is a dopamine receptor agonist that inhibits pituitary prolactin secretion
how to achieve fertility in women with ovulatory failure who are normogonadotropic, normoprolactinemic, euthyroid ????
clomiphene citrate is an Antioestrogen that stimulates ovulation by blocking the feedback inhibition of oestrogen on the hypothalamus thereby enhancing the release of pituitary gonadotropins
How to stimulate ovulation in women who have hypothalamic GnRH secretion ? (hypogonadotropic, hypogonadal anovulation)
Pulsatile GnRH infusion can stimulate ovulation.
pituitary and ovarian function must be intact for this method to work
How can Turner’s syndrome (45, XO) patient get pregnant/method?
After checking renal cardiac and thyroid examinations.
IVF
notes:
Most women are infertile secondary to ovarian failure.
With sufficient oestrogen and progesterone supplementation, these woman can develop a thick endometrial lining that is substantial enough to support a pregnancy.
best if ovum from a donor!!! (60%)
If occurs spontaneously there will be an increased risk of spontaneous abortion , down syndrome and Turner syndrome
how to achieve fertility in women with ovulatory failure who are normogonadotropic, normoprolactinemic, euthyroid ????
clomiphene citrate is an Antioestrogen that stimulates ovulation by blocking the feedback inhibition of oestrogen on the hypothalamus thereby enhancing the release of pituitary gonadotropins
How to stimulate ovulation in women who have hypothalamic GnRH secretion ? (hypogonadotropic, hypogonadal anovulation)
Pulsatile GnRH infusion can stimulate ovulation
What can hCG therapy do?
trigger the ovulatory cascade in an oocyte donor when her follicles are deemed mature.
turner syndrome characteristics 10 points
- Narrow, high arched palate
- low hairline
- webbed neck
- broad chest with widely spread nipples
- cubitus valgus
- short stature
- coarctation of aorta
- bicuspid aortic valve
- horseshoe kidney
- streak ovaries, amenorrhea and infertility
How to stimulate ovulation in women who have hypothalamic GnRH secretion ? (hypogonadotropic, hypogonadal anovulation)
Pulsatile GnRH infusion can stimulate ovulation
what is karyotype of turners syndrome + mechanism
45, XO
loss of paternal chromosome X
Congenital adrenal hyperplasia (adrenogenital syndrome)
what is it and MOST COMMON TYPE?
-Abnormal sexual differentiation due to defective hormone synthesis in the adrenal glands
21 – hydroxylase deficiency is the most common
-At birth patients have ambiguous genitalia (girls only) and salt wasting (hypertension, hyponatraemia)
Androgen insensitivity syndrome
defect?
typical karyotype ?
appears?
results from a defect in testesterone receptors.
GENETICALLY MALE ;46, XY adolescent who appears phenotypically female (d/t resistance to testesterone) but has primary amenorrhea d/t the absence of an internal female reproductive tract (MULLERIAN STRUCTURES) and the presence of cryptorchid testes (secrete testesterone)
BREAST DEVELOPMENT results from peripheral conversion of testosterone to oestrogen, but axillary and pubic hair is absent.
NO penis/scrotum
No uterus/ovaries
Edward syndrome cause and presentation
trisomy 18, caused by meiotic nondisjunction. they have multiple anomalies, including cardiac defects, clenched fists, rocker bottom feet, omphalocele, and low set ears
cri du chat cause and presentation
due to de novo partial deletion of the short arm of chromosome 5 (5p-)
typically have round face, catlike cry, and microcephaly.
Down syndrome causes (2) + presentation
1- meiotic nondisjuntion
2- robertsonian translocation
flat face, oblique palpebral fissures, and epicanthal folds.
what is the most common cardiac anomaly in down syndrome
atrioventricular defects
how does turner syndrome manifest in neonate
1- lymphedema (swelling)
2- cystic hydromas (neck)
short stature, primary amenorrhea, aortic anomalies
What is an imperforate hymen
It is an obstructive lesion caused by incomplete degeneration of the central portion of the fibrous tissue band connecting the walls of the vagina.
At birth, vaginal secretions stimulated by the mothers oestrogen can cause a mucocolpos (accumulation of mucus in the vaginal canal) which may manifest as a bulging introitus.
if the condition remains undiagnosed, the mucus is reabsorbed and the child will be asymptomatic until menarche.
how does a patient with imperforate hymen present?
-primary amenorhhea!!! and normal secondary sexual charecteristic with CYCLIC! abdominal or pelvic pain!! due to the accumulation of menstrual blood in the vagina and uterus (e.g hematocolpos!!!)
the pressure from the resulting collection of blood can also cause back pain and difficulties with defecation.
secondary sexual development!! is normal as the pt has NO chromosoamal or hormonal abnormalities.
imperforate hymen examination shows :
vaginal bulge and/or mass palpated anterior to the rectum
Asherman syndrome leads to what?
causes SECONDARY amenorhhea through obstruction from scarring of the uterine cavity .
this is typically a sequela of uterine infection (e.g postpartum endometritis) or procedures (e.g. dilation and curettage)
What is endometriosis
The presence of endometrial glands and stroma outside the uterus.
Can endometriosis cause amenorrhea
NO only severe dysmenorrhea with lower abdominal cramps that begin 1-2 days before menses.
What is it common site of endometrial implants
pouch of Douglas which presents as painful defecations, dysparunia, amd palpable nodularity on rectovaginal examination
What is the most common cause of primary amenorrhea
turner syndrome
Can Turner syndrome patient develop secondary sexual characteristics
No
What is Kallmann syndrome and how does it present
Impaired synthesis of gonadotropin- releasing hormone by the hypothalamus.
presents with:
1- primary amenorrhea
2- absent secondary sexual characteristics.
3- olfactory sensory defect
in what phase is progesterone secreted (menstrual period)
luteal phase
fxn of progesterone in period
stimulates the endometrium to transform from proliferative to secretory to become a hospitable environmen for embryonic implantation
—> endometrial glands become more elaborate
and the spiral arteries coil
taking exogenous progesterone for 10 days , do what?
matures the endometrial lining
explain menstrual flow
-endometrium no longer exposed to progesterone
(or could be progesterone withdrawal test!!!)
-prostaglandin production increases, leading to VASOCONSTRICTION of the spiral arteries!!!
also:
-progesterone withdrawal also causes increased secretion of metalloproteases by endometrial stromal cells (casuing degradation of the extracellular matrix and APOPTOSIS!!! of the endometrial epithelium .
Net effect: degeneration of the functionalis layer, which sloughs away as menstrual flow
what is dysplasia
abnormal growth of cells, tissues, or organs
e.g transformation zone of the cervix
what is granulation
process of scar formation that involves deposition of connective tissue and angiogenesis
why women with Asherman syndrome dont bleed (no progesterone withdrawal bleeding)
because the endometrium is essentially replaces with scar tissue
what is hyperplasia
what is hypertrophy
- enlargement of tissue or an organ d/t an increase in the number of cells
- enlargment of tissue or organ d/t increase in the size of its cells
in what dx is uterine hypertrophy seen?
ADENOMYOSIS
What is the primary hormone responsible for stimulating the endometrium (to be suitable for implantation)
progesterone
what is fibroadenoma ?
age?
MOST COMMON benign tumor of the breast
-YOUNG WOMEN 15-35
describe fibroadenomas
nodules that are well-demarcated,painless, mobile, and spherical, 1-10 cm in size.
they can also occur as multiple and/or bilateral lesions
how young vs old women discover fibroadenoma
young: usually discovered as palpable mass by pt/physician
old: incidentally or mammography
when do fibroadenomas increase/decrease in size?
increase: 1- pregnancy 2- lactation 3- with estrogen therapy decrease: 1- after menopause
histology of fibroadenomas
benign-appearing cellular or myxoid stroma!!!!!
that encircles epithelium-lined glandular and cystic spaces.
-well defined border
but may compress/distort surronding glandular epithelium
what happens to fibroadenomas as women age
epithelium atrophies and the stroma becomes more hyalinized
what is DCIS
malignant clonal cell proliferation CONTAINED by the surrounding ductal basement membrane.
what layer is preserved in DCIS
-the basal (myoepithelial) layer of the duct is preserved and uninvolved
characteristics of mammary duct ectasia
- ductal DILATATION
- inspissated breast secretions
- chronic granulomatous inflammation in the periductal and interstitial areas
medullary carcinoma of the breast
characterized by:
- solid sheets of vesicular, pleomorphic, mitotically active cells
- significant lymphoplasmacytic infilitrate (around and within) the tumor.
- pushing, noninfiltrating border
what is paget disease OF THE NIPPLE ?
physical exam?
rare breast cancer malignant cells spread from superficial DCIS into nipple skin without crossing the BM. —> shows: 1- unilateral erythema 2- scale crust around the nipple
what is sclerosing adenosis ?
COMMON FINDING IN: fibrocystic changes
characterized by:
central acinar proliferation and compression with surrounding fibrotic tissue and peripheral ductal dilation
risk factors of epithelial ovarian cancer
1- FHx 2- infertility (ovarion dysfunction)** 3- nulliparity ** 4- polycystic ovarian syndrome 5- endometriosis 6- BRCA1/2 MUTATIONS ** 7- lynch syndrome 8-post menopausal hormone therapy
protective factors of epithelial ovarian cancer
1-Combined OCP** 2- multiparity ** 3- breastfeeding** 4- salpingo-oophorectomy sos: they decrease the frequency of ovulation, i.e less trauma and repair
- abdominal distension
- ascites
- pleural effusion
- bowel obstruction
- decreased appetite
- weight loss
- ovarian mass
Epithelial ovarian cancer (EOC)
ovarian cancer marker
is it sensitive/ specific ?
Cancer Antigen 125
CA-125!!!!
produced by ovarian epithelia
it is NEITHER sensitive nor specific for early EOC (can be found in normal tissue and other ca)
why nulliparity is a risk factor for ovarian cancer
it means repeated ovullation
why nulliparity or infertility lead to ovarian cancer?
they inflicit minor trauma to the ovarian surface, therefore rendering the epithelia susceptible to transformation
to what cancers is HPV infection linked?
cervical
vaginal
vulvar
NOT OVARIAN
long term antioxidant supplementation (VITAMIN C) and cancer risk
antioxidant neutralize reactive oxygen species ROS and free radicals, so they decrease damage to cells.
answer: not proven yet :)
GENITAL DEVELOPMENT NOTES remember: <6 wks 2 pairs of genital ducts: 1- paramesonephric (mullerian) 2- mesonephric (wolfian)
UNDIFFERENTIATED GONAD —>
XX or XY
ovary or Testis
OVARY /// passive wolffian duct regression (d/t lack of hormonal stimulation) estrogen —> mullerian duct: by 20 wks 1- fallopian tubes 2- uterus /cervix 3- upper vagina
TESTIS /// AMH —> active mullerian duct regression testesterone —> wolfian duct: 1- epididymis 2-vas deferens 3- seminal vesicles
mullerian aplasia
aka vaginal agenesis
or Mayer-Rokitansky-Kuster-Hauser (MRKH) syndrome
SOSOSOSOS
they have:
- Variable uterine development !!!
- No upper vagina !!! (e.g short vagina)
- uterus is hypoplastic/ absent, thus pts cannot menstruate ( primary amenorrhea) !!!
- normal ovaries: secrete estrogen —> regular development of secondary sexual characteristics (breast, pubic hair)
all females with mullerian defect should check what
renal ultrasound (50% have coexisting urologic anomaly) e.g unilateral renal agenesis !!
what deficiency is most common in congenital adrenal hyperplasia ?
21- hydroxylase deficiency
how does late onset 21- hydroxylase deficiency present?
- hirusutism
- oligomenorrhea
- acne
Klinefelter syndrome (47,XXY) characteristics -affects males
- tall stature (long legs)
- poorly developed secondary sexual characteristics (no facial/body hair)
- atrophic testes
- infertility
- intellectual disability
- gynecomastia
47, XXX characteristics
-tall stature
- slightly decreased IQ scores
- normal physical features
(including sexual development)
female sexual interest/arousal disorder.
diagnosis?
- diagnosis requires rulling out:
1. psychological
2. medical
3. substance/medication related causes
(e. g depression, diabetes, chronic alcohol or drug use)
4. relationship problems
female sexual interest/arousal disorder.
what is it?
1- decreased interest -lack of sexual thoughts -reduced initiation of sexual activity -receptivity to a partners attempts to initiate BUT ADEQUATE LUBRICATION/ORGASM
2- decreased arousal
-decreased excitement/pleasure in response to mental or physical cues.
3- both
SSRI and Noreepinephrine-dopamine reuptake inhibitor
effect on sexual activity
SSRI/ SNRI
cause medication induced sexual dysfunction or
decreased libido or
anorgasmia in women
NDRI (e.g bupropion)
doesn’t affect serotonin
unlikely to cause sexual side effects
female orgasmic disorder definition
-marked delay in, decreased frequency, and intensity of orgasms
or
-absence of orgasm
genitopelvic pain/penetration disorder
involves recurrent difficulties with pain or fear of pain with vaginal intercourse or penetration attempts
how menopause affects sexual activity?
hint: estrogen
peri- and post-menopausal (declining levels of estrogen) may be associated with decreased sexual interest..
accompanies by:
-decreased lubrication !!
clinical feautures of gonococcal cervicitis
- purulent or mucopurulent discharge
- friable cervix with easy bleeding
(e. g. intermenstrual or postcoital bleeding)
classically ASYMPTOMATIC
diagnosis of gonococcal cervicitis / testing
Nucleic acid amplification testing !!!!!
treatment of gonococcal cervicitis
3rd generation cephalosporins
PLUS
azithromycin or doxycycline
untreated; cervicitis :
bacterias and complications
N. gonn and Chlam trach
ascends to the upper genital tract causing PID
leading to ectopic pregnancy or infertility
how PID cause infertility
sos
results in tubal factor infertility d/t scarring of the fallopian tube!!!
are gonococcal and chlamydial infections RF to cervical cancer?
no
effect of ocp on ovarian cancer
decreased risk
is cervicitis RF for ovarian ca
no
EFFECT OF OBESITY/ ESTROGEN ON ENDOMETRIAL HYPERPLASIA
elevated estrogen w/o opposition by progesterone stimulates growth of the uterine lining
w/ OBESITY , there is an INCREASED risk of AROMATIZATION of androgens to estrogen in the adipose tissue :)) !!
endometrial sampling showing:
- coiled glands filled with carbohydrate-rich mucus
- edematous stroma
- tortuous spiral arteries
what phase of the period?
secretory phase (b/w ovulation and menses) days:15-28
secretory phase endometrial biopsy
—> progesterone released by the corpus luteum causes the UTERINE GLANDS to:
-coil (and increase in size)
-cells lining the glands acquire large cytoplasmic vacuoles.
-secrete glycogen-rich mucus (in preperation to embryo implantation)
—> ENDOMETRIAL STROMA become edematous and completely traversed by tortuous spiral arteries that extend from the deeper layers to the uterine lumen (endometrial surface)
uterine endometrium anatomy revision
upper layer: stratum functionale
consists of lamina propria (studded with tubular glands), spiral arteries and dilated capillaries.
what marks the beginning of the proliferative phase and when does it end?
BEGINS: first day of menses
ENDS: with ovulation
what is the function of estrogen in the proliferative phase?
stimulates proliferation of the stratum functionale
how does the endometrium looks during proliferative phase?
-non branching, non budding, uniform GLANDS.
evenly distributed throughout a uniform STROMA
midprolifertaive phase biopsy of the endometrium
- glands are tubular, narrow, and lined with pseudostratified, elongated mitotically active epithelial cells.
- startium functionale: contains compact, NONedematous stroma
- uterine glands in length and girth but still remain relatively straight
- no secretions are present in the glandular lumens
- endometrium thickens, BUT the coiled spiral arteries remain limited to the deeper layers.
endometrial biopsy at ovulation
shows late proliferative endometrium with coiled glands and occasional cytoplasmic vacuoles in the glandular epithelium
- painful urination
- urinary frequency/urgency
- suprapubic tenderness
- NO FEVER,FLANKPAIN, COSTOVERTEBRAL ANGLE TENDERNESS
ACUTE CYSTITIS
how CYSTITIS arise?
fecal organisms!!!!! gain access to urethral meatus and ascend to bladder
most common causes(bacterias) of cystitis
- E.coli 70% -gram -ve coliform bacteria
- other Enterobateriaceae (less common)
- Klebsiella pneumonia
- Proteus mirabilis
why do women develop UTI more common (2)
1- proximity of the anus and vaginal introitus
2-short length of female urethra
most common cause (bacteria) of vulvovaginitis
Candida albicans
- vaginal discharge
- burning
- PRURITIS
vulvovaginitis
STDs in symptomatic women
sos this symptom
SIGNIFICANT mucopurulent vaginal discharge
- asymptomatic
or
-thin whitish vaginal discharge
-FISHY vaginal odor
Bacterial vaginosis
what is the normal vaginal flora (e.g) ad in what dx it is replaced and with what?
normal (e..g Lactobacillus)
is replaced by facultative anaerobes (e.g Gardnerella vaginalis) in bacterial vaginosis
what colonizes the genital and GI tract? so rarely cause infections
group B streptococcus
early neonatal sepsis cause
group B streptococcus passed to infants during vaginal birth
what women are more susceptible to get UTI by uncommon UTI organisms:
1- Pseudomonas aeruginosa
2- Staphylococcus
although E.coli is still more common !!!
1-recently received antibiotics
2-have been hospitalised
enteric pathogen
E.coli
mos common cause of genital herpes
HSV-2 !!
-cluster of PAINFUL vesicles, pustules and/or ulcers on:
labia, penis, buttocks, or THIGH
+/- systemic symptoms in primary infection
(fever)
genital herpes
tx of genital herpes
Acyclovir,
famciclovir, or
valacyclovir
- systemic symptoms (fever, myalgia)
- inguinal lymphodenopathy !!!
- itchy, painful, vesicular genital rash
PRIMARY genital herpes !!
what is the course of the characteristic rash on the genitalia or buttocks
STAGES
vesicular—> ulcers —> crusting !!!
following infection, where does HSV remain dormant
sacral dorsal root ganglia
which is stronger primary or recurrent HSV
recurrence is more localized and less severe due to humoral immunity
when is HSV more contagious
during RECURRENCE
do contraception preven HSV spread
YES
What is a neurological manifestation of lyme disease
Facial nerve palsy
what causes lyme diseases
sphirocete Borrelia burgdorferi
or HSV-1
HSV-1
oral vs genital
ORAL MORE
-fatigue
-anorexia
-headache
-occasional fever
WITHOUT a vesicular rash
Lyme disease
untreated syphilis —> tertiary neuro manifestations ?
infects the dorsal roots of the spinal column and lead to tertiary neurosyphilis characterized bt:
1- tabes dorsalis (locomotor ataxia)
2- general paresis
how does primary syphilis present
SINGLE painless genital lesion (CHANCRE) after intital infection with Treponema pallidum sphirocete)
Varicella zoster virus effect on neuro
ALSO (like syphilis) invades the dorsal root sensory ganglia.
and reactivation causes herpes zoster (e.g shingles)
neurological complication of shingles
Postherpetic neuralgia (persistent pain after resolution of lesions)
typical presentation of herpes zoster is
SOS
PAINFUL vesicular rash in a dermatomal distribution
WITHOUT systemic involvement
HPV human papillomavirus what is it? what type of cells it infects? what cancers? skin manifestation?
- oncogenic double-stranded DNA virus
- infects EXCLUSIVELY epithelial cells.
- predispose cervical, vulvar carcinoma
- WARTS
DD (what is the dx? organism? tx?
DISEASE 1
-thin, off-white discharge with fishy odor
-no inflammation (no redness, pruritis)
-(pH>4.5, clue cells, +ve whiff test: amine ofor with KOH)
DISEASE 2
-thin, yellow-green malodorous, frothy discharge
-vaginal inflammation
-(pH >4.5, motile trichomonads)
wet mount: leukocytes and PEAR-shaped organisms: flagellated trophozoites)
*cervix w/ punctate hemorrhage : STRAWBERRY CERVIX
DISEASE 3
-Thick, “COTTAGE CHEESE” discharge
-Vaginal inflammation
-(NORMAL pH 3.8-4.5, pseudohyphae)
DD of vaginitis DISEASE 1 -bacterial vaginosis -gardnerella vaginalis -Metronidazole or clindamycin
DISEASE 2
- Trichomoniasis
- Trichomonas vaginalis)
- Metronidazole, TREAT sexual partner
DISEASE 3
- Candida vaginitis
- candida albicans
- fluconazole
association for bacterial vaginosis
- smoking
- sexual activity
- vaginal douching
why vaginal pH increases in bacterial vaginosis !!!!
decreased lactobacilli colonization
what causes fishy smell in bacterial vaginosis?
anaerobic bacterias (e.g gardnerella vaginalis) generates malodouros amines
amines lead to:
1- GRAYISH WHITE
2- FISHY SMELLING
what are clue cells !!
clue cells : SQUAMOUS epithelial cells with adherent bacteria.
shown in Wet mount microscopy of bacteria in bacterial vaginosis shows
what is positive whiff test and in what disease
in bacterial vaginosis
-application of potassium hydroxide to the discharge produces an amine odor ;)
wet mount microscopy of normal vaginal discharge (physiologic leukorrhea) shows:
note: it is not malodourous
epithelial cells and rare leukocytes
-cervical erythema
-friability
-purulent cervical discharge
what type of bacteria?
N. gonorrhea cervicitis
gram -ve intracellular diplococci
underlying mechanism of turner syndrome
meiotic nondisjunction !! during gametogenesis
NOTE : if the nondisjunction occurs during mitosis early in embryogenesis :::
: mosaic turner syndrome can be (45,X &46,XX) one X will be structurally abnormal and missing some genetic material (e.g X fragments, isochromosomes)
what gene is missing in turner syndrome? and its fxn?
SHOX gene!!!! which promotes long bone growth , thus pts have short stature!!!
meiotic nondisjunction occurs in what syndromes?
Turner syndrome
Klinefellter syndrome
trisomies 13,18,21
what is a balanced translocation?
clinically silent as there is no excess or shortage of genetic material.
what is the risk of a balanced translocation?
a parent with a balanced translocation is at risk for having a child with an unbalanced translocation.
e.g 3-4% down syndrome pts: (unbalanced trisomy 21)
in which one chromosome 14 contains the long arms of both chromosomes 14 and 21
what is a frameshift mutation
is a genetic mutation in which a number of nucleotides not divided by 3 are inserted into or removed from a coding DNA sequence.
so the reading frame is shifted during protein translation, resulting in an entirely different peptide sequence (typically w/ formation of a premature stop codon)
give 3 examples of dx’s with trinucleotide repeat expansion
fragile x syndrome (CGG repeats) myotonic dystrophy (CTG repeats) Huntington disease (CAG repeats)
what is uniparental disomy?
and examples
individual inherits 2 copies of a chromosome from one parent only.
1- angelman syndrome
2- prader-willi syndrome
(on chromosome 15 both)
turner syndrome 3 types of karyotype
45,X complete monosomy
45,X/46,XX mosaicism
46,XX w/ partial deletion of one x chromosome
proteins in gap junction + fxn
Connexins
-intracellular communication
proteins in tight junction + fxn
Claudins, occludin
-paracellular barrier (to water and solute)
proteins in adherens junction + fxn
Cadherins
-cellular anchor (similar to desmosomes and hemidesmosomes)
proteins in desmosomes + fxn
Cadherins
(e.g desmogleins, desmoplakin)
-cellular anchor
(similar to adherens junction and hemidesmosomes)
proteins in hemidesmosomes + fxn
Integrins
-cellular anchor (similar to desmosomes and adherens junction)
what type of cell junction is important during labor?
gap junction
effect of estrogen on cell junction (during labor)
Immediately prior to delivery, estrogen stimulates upregulation of gap junctions !!!! between individuals myometrial smooth-muscle cells.
this heightens myometrial excitability !!
note: gap junctions consist of aggregated connexin proteins (e.g. connexin–43) that allow passage of ions between myometrial cells.
effect of estrogen on oxytocin receptor (during labor)
oxytoocin receptors are uterotonic receptors. which mediate calcium transport through ligand-activated calcium channels
2 requirements to have a coordinated, synchronous labor contractions
1- increase in gap junction density
2- uterotonic (oxytocin) receptors
both adherens junctions and desmosomes are composed of cadherins
what are the different cytoplasmic anchors?
- adherens junction: actin filament
- desmosomes: intermediate filament
Autoantibodies agains desmoglein
(a cadheren protein for desmosome) found in what disease
pemphigus vulgaris
what are fenestrae?
gaps b/w endothelial cells that allow for paracellular transport.
new-onset hypertension
proteinuria
end-organ dysfuction
at >/= 20 wks gestation
+ pathophysiology
preeclampsia
Swollen fenestrae in renal glomerular capillary endothelial cells
Autoantibodies against hemidesmosomes leads to: 2:
1- bullous pemphigoid
2- pemphigoid gestationis
how tight junctions are connected to food poisoning?
enterotoxin from clostridium perfringens (common cause of food poisoning) binds CLAUDIN.
so water loss from the tissue to the interstitial lumen results in WATERY DIARRHEA
- lower abdominal pain (pelvic cramping)
- vaginal bleeding
- positive pregnancy test (e.g detectable b-hCG) !!
- palpable adnexal mass !!!
ECTOPIC PREGANNCY
locations of ectopic pregnancy
and whats the most common
1- tubal (most common 90 %) in the fallopian tube!! 2- cornual/interstitial 3- ovarian 4- abdominal 5- cervical
give example of tubal pathology that often cause ectopic pregnancy (2)
1- PID
2- prior pelvic surgery
how tubal ectopic pregnancy leads to the classic symptoms of pelvic cramping! and vaginal bleeding! (e.g spotting)?
it develops into a highly vascular adnexal mass that draws BF from surrounding tissues to maintain its rapid growth.
this causes:
- ischemic injury to surrounding tissues
- fallopian tube edema and potential tubal rupture
hydatidiform mole typical presentation
-enlarged uterus d/t abundant growth of chorionic villi
-markedly elevated b-hCG (>100,000 mIU/mL)
note:
adnexal enlargement (theca lutein cyst formation d/t b-hCG stimulation)
are fibroids associated with b-hCG?
no
uterine fibroids locations
1- intracavitary 2- submucosal 3- intramural 4-subserosal 5- pedunculated (in order from inside to outside)
what is endometrioma
ectopic endometrial tissue in the ovary
*can cause adnexal mass and vaginal bleeding if ruptured
*dysmenorrhea and endometriosis symptoms (dyspareunia, dyschezia)
*adnexal mass
+/- vaginal bleeding
endometrioma +/- rupture
what is mature teratoma
ovarian mass composed of
ectoderm
endoderm
mesoderm
pt with a mature teratoma are at risk of what?
ovarian torsion
- pelvic pain
- palpable adnexal mass
- SUDDEN and UNILATERAL pain
- uncommon vaginal bleeding
OVARIAN TORSION
task
sos
google how candida looks in wet microscopy :)
and clue cells in BV
and trichomonias
what can cause an imbalance in the normal vaginal flora
i.e excessive candida (usually a bit) ?
and list some risk factors
—> increased estrogen levels !!! e.g:
1- estrogen containing contraceptive use
2- pregnancy
risk factors: 1- antibiotic use !!! 2- immunosuppression (e.g systemic corticosteroids) 3- sexual activity 4- DM (esp if poorly controlled) !!!
how is candidal vulvovaginitis diagnosed?
wet mount microscopy
reveals pseudohyphae with budding yeast and true hyphae
MoA of azole (antifungake med)
FLUCONAZOLE?
DECREASE ergosterol synthesis
and dirsupt fungal cellular membrane formation
tx of herpes simplex virus
acyclovir
how is herpes simplex virus visualized
cervical CYTOLOGY (not wet mount microscopy) shows multinucleated giant cells
can HSV cause cervicitis?
RARELY
what abx is azithromycin
macrolide
what abx is ceftriaxone
3rd gen cephalosporins
why C. trachomatis cannot be easily visualized in microscopy?
d/t its unusal peptidoglycan cell wall
pt with INTERMITTENT leakage of urine likely has
+leakage during valsalva maneuver
Stress urinary incontinence
SUI
how pelvic floor muscles maintain continence in women? !!
- contract to stabilise the urethra against the anterior vaginal wall
- this decreases the angle b/w the bladder neck and the urethra (urethrovesical angle)
- thereby compress the urethra, stopping urine flow
how the pelvic floor muscles become weak ? !!!
chronically increased intraabdominal pressure
-obesity
-chronic cough from COPD !!!!!
ALSO
-prior pregnancies!! (incl cesarean)
it increase the laxity of pelvic floor muscles and CT.
stress urinary incontinence tx
pelvic floor muscles (i.e kegel) exercises and pessary placement (help support and maintain normal pelvic anatomy)
most common cause of vesico-vaginal fistula
bladder injury from surgical or obstetric complications (e.g operative vaginal delivery)
- CONTINUOUS urinary dribbling
* leakage of urine from VAGINA (not urethra)
vesico-vaginal fistula
bladder
sympathetic vs parasympathetic
sympathetic:
- promotes urine storage &continence (by increasing urethral sphincter tone)
parasympathetic:
- stimulates detrusor muscle contraction and micturition
sos fill: cholesterol —> androgens —> estrogen in what ovary cell types these steps take place or note:
cholesterol —> progesterone
cholesterol —in THECA INTERNA—> androgens —IN GRANULOSA CELLS(contain enzyme: aromatase)—> estrogen (estradiol)
extra promotions:
- LH increases synthesis of androgens (and progesterone) in theca interna
- FSH increases synthesis of estrogen
what is the predominant estrogen in the human body
estradiol (derived from ANDROGENS)
what is the role of theca externa ?
is it involved in steroidgenisis?
NO,
composed of a layer of SM and fibroblast cells.
so connective tissue support structure for the follicle :)
female oocyte timeline
- embryogenesis:
- ovulation:
- fertilization:
- embryogenesis: formed here and remain arrested in prophase 1 until ovulation.
- ovulation: single oocyte completes meiosis I
- fertilization: meiosis II occurs
where are leydig cells found?
analogues to what in the other gender?
MALE testes only
analouges to theca interna cells of the ovarian follicle.
i.e stimulated by LH to secrete testosterone
HPV STRAINS PRESENTATION
1-4
6,11
16,18
1-4: skin warts (verruca vulgaris) e.g plantar wart
6,11: genital warts (condylomata acuminata)-low malignancy potential
16,18 (and 31!!): cervical, vaginal, vulvar and anal neoplasia
most common type of cervical cancer
SCC
arises from teh squamocolumnar junction of the endocervix
what is CIN ?
dysplasia d/t —
!!!!!!
cervical intraeoithelial neoplasia is CARCINOMA IN SITU , precedes SCC.
dysplasia d/t HPV
what women are at risk of invasive cervical cancer ?
- persistent HPV infection
- Untreated high-grade CIN
How high risk strains of HPV cause malignancy
when high-risk strains (16,18,31) enter human cell genome, lead to overexpression of viral oncogenes E6 and E7. !!!!
- E6 binds protein p53 and increases its degradation
- E7 bind the retinoblastoma (RB1) gene and displaces transcription factors normally bound by pRB (tumor suppressor protein product of RB)
Cervical cancer RF are related to what RF?
the risk of acquiring HPV infection
- hx of multiple partners
- lack of barrier contraceptive (e.g condom) use !!!
alcohol increases risk of what cancer
Liver
Breast
Nulliparity, early menarche, obesity increases risk of what cancer
and why
endometrial cancer (these factors are associated with increased estrogen stimulation of the endometrium )
DOUCHING is a risk factor of
Bacterial vaginosis
-disrupts the vaginal ecosystem resulting in overgrowth of gardnerella vaginalis
LYMPH NODE DRAINAGE of the female reproductive system
- Uterus
- Cervix
- Vagina
- Vulva
- Ovaries
- Uterus: external iliac (oUT: EXit)
- Cervix: internal iliac (SIR plz ENTER)
- Vagina:
proximal: internal iliac
distal: inguinofemoral - Vulva: inguinofemoral ! (VU the pENGUIN)
note: superficial inguinal and deep femoral - Ovaries: paraaortic (OOvary aOOrta)
most common type of vulvar cancer
SCC
- ulcerative lesion or
- plaque on the LABIA
vulvar cancer !!
RFs of vuulvar cancer (3)
1- chronic HPV infection
2- prior vulvar lichen sclerosus
3- tobacco use
what is sentinel lymph node biobsy? !!
first lymph nodes to drain th PRIMARY tumor site
what is the lymph drainage of the lower extremities, buttocks and external genitalia) ?
lymph from:
- uterine corpus
- inguinal nodes
these drain to the external iliac nodes
then, external + internal drain to common
lymph drainage of the bladder, uterus, and cervix
obturator nodes (located in the obturator fossa medial to the external iliac vessels.
pelvic lymph node groups 1- obturator 2- external iliac 3- internal iliac drain all together:
pelvis
lower extremities
lower abdominal wall
where does the common iliac drain to
paraaoric lymph nodes
lymph drainage of anal canal amd rectum
presacral lymph nodes
