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FEMALE reproductive > female uworld > Flashcards

female uworld Flashcards

1
Q

PID causes (bacterias)

A

N. gonorrhea

C. trachomatis

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2
Q

Pelvic inflammatory disease
TX?
complications ? (IF DID NOT RECEIVE FULL TX TOO)

A

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
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3
Q

Fitz-Hugh-Curtis syndrome

A

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.

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4
Q

most common cause of tubal factor infertility

A

PID

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5
Q

fever
(lower) abdominal pain
mucopurulent cervical discharge

A

PID

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6
Q

low sperm volume and acidic pH of an ejaculate sample means

A

congenital absence of the vas deferens

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7
Q

is oral contraceptive use associated with OVARIAN FAILURE ?
if not, what is associated?

A

NO !!
-smokers or
- receiving radiation or chemotherapy
is related to premature ovarian failure (i.e. primary ovarian insufficiency

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8
Q

what is the role of oestrogen and progestin in oral contraceptive pills?

FUN FACT: if used as prescribed: reliable and reversible :)

A

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
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9
Q

side effects of oral contraceptive pills

A
  • 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
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10
Q

does past pregnancy or childbearing status affect OCP side effect?

A

NOOOOOO

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11
Q

is OCP contraindicated with DM?

A

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)

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12
Q

effect of HDL and LDL levels with OCP use. what are the contraindicated?

A

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
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13
Q

ABSOLUTE CONTRAINDICATIONS TO THE USE OF OCP are: (6)

A

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

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14
Q

what is “COMPLETE” molar pregnancy ?

A

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

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15
Q

risk factors of molar pregnancies

A

1- extremes of maternal age
2- prior molar pregnancy
3- prior miscarriage
4- infertility

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16
Q

most common type of complete mole (molar preganncy) — 90%?

and whats less likely?

A

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

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17
Q

what is the most common sex xhromosome abnormality in females?

A

47, XXX (incidentally found)

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18
Q

what is 47, XXY karyotype means?

A

Klinefelter syndrome

associated with hypogonadism in males

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19
Q

what causes klinefelter syndrome? 47, XXY

A

non disjunction of the sex chromosomes during meiotic division of the gamete of wither parent

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20
Q

what are partial molar pregnancies?

A

69, XXX OR 69, XXY
fertilization of an ovum with 2 sperms

  • it contains fetal tissue and normal placental villi intermixed with hydropic villi
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21
Q

postpartum hemorrhage cause

A

failure of the uterus to contract and compress the placental site blood vessels. leading to uterine atony!!!

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22
Q

postpartum hemorrhage risk factors

A

1- prolonged labour

2- twin gestation

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23
Q

tx of postpartum hemorrhage

A

1- uterine massage
2- uterotonic medications (oxytocin)
3- fails—> surgery

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24
Q

what is the main supply of the pelvic organs? and uterus?

A

internal illiac arteries (hypogastric arteries)

branches to give uterine arteries

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25
Q

postpartum hemorrhage surgery goal

A

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

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26
Q

ANATOMY REVIEW BF

A

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

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27
Q

what happens if an injury to the pudendal artery happens during vaginal delievery ?

A

vulvar hematoma

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28
Q 
Heavy prolonge menses
pelvic pain 
constipation
urinary frequency 
enlarged irregular uterus 
obsetric complications
A

uterine leiomyomas

FIBROIDS

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29
Q

what are uterine fibroids

A

BEINIGN

monoclonal SM tumors (that develop within the myometrium)

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30
Q

major risk for fibroids

A

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

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31
Q

is there a correlation between ovarian ca family hx and fibroids

A

NO

remember ca: large immobile ovaries

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32
Q

what cancer u can get if u work in a textile factory ?

A

BLADDER CANCER (EXPOSURE TO CARCINOGENS)

symptoms:
- increased urinary frequency
- concomitant hematuria

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33
Q

progestin-only pill and fibroids relation ?!

A

used in symptomatic fibroids to decrease their size :)

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34
Q

prior deliveries increases the risk of what ? (increased parity)

A

1- adenomyosis
-pelvic pressure
-symmetrical enlarged tender globular uterus
2- endometrial tissue with the myometrium

3- DECREASED RISK OF FIBROIDS

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35
Q

red meat consumption increases risk of uterine ————?

A

fibroids

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36
Q

pts with symptomatic uterine fibroids are often treated ——

A

surgically with a hysterectomy

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37
Q

how does a fibroid appear grossly?

A

discrete, yellow-gray tumors !!

with a think pseudocapsule that separates the fibroid from the normal uterine myometrium

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38
Q

why fibroids lead to HEAVY MENSES???

A

because they increase the endometrial surface area (d/t mass effect) :)

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39
Q

how do we confirm fibroids (uterine leiomyoma) diagnosis?

A

confirmed with MICROSCOPY

reveals monoclonal proliferation of myocytes and fibroblasts !!

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40
Q

how do we confirm fibroids (uterine leiomyoma) diagnosis?

A

confirmed with MICROSCOPY
reveals monoclonal proliferation of myocytes and fibroblasts !!
because each fibroid arises from a single progenitor SM cell.

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41
Q

how does cervical ca present?

A

asymptomatic or

irregular, postcoital spotting (NOT HEAVY MENSES!!!)

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42
Q

where is cervical ca typically found?

A

in the cervical transformation zone

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43
Q

how does cervical ca look under microscope ?

A

dysplastic squamocolumnar cells with areas of atypia

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44
Q

how does endometriosis typically present? what is it

A

-painful menses (dysmenorrhea)

—> endometrial tissue implants outside the uterus!! rather than intrauterine mass (i.e in fibroids)

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45
Q

how is endometriosis seen microscopically

A

ectopic endometrial glands!! and hemosiderin-laden macrophages

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46
Q

how does pts with endometrial hyperplasia or cancer typically present?

A

-irregular, heavy menses
-thickened endometrium
(in fibroids its a mass in the myometrium)

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47
Q

histopathology of endometrial hyperplasia or cancer:

A

hyperplastic proliferation of irregular endometrial glands

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48
Q

microscopy of ovarian cancer>?

A

infiltration of the stroma by high-grade serous carcinoma.

note ovarian ca causes an adnexal mass!! rather than a solitary intrauterine mass(in fibroid)

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49
Q

describe peau d’orange rash

A

generalized, erythematous!!, may be tender or itchy.

skin texture: firm! and coarsely pitted! like an orange peel

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50
Q

inflammatory breast cancer !!!

A

PEAU D’ORANGE (w/ or w/o breast mass) and BREAST EDEMA!!

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51
Q

DVT causes

A

occurs due to hypercoagulability related to malignancy, surgery, or IV catheter placement

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52
Q

Can DVT affect upper extremities

A

yes, it presents with oedema and pain in the affected lamp

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53
Q

What happens if silicone breast implant ruptures

A

Lead to a foreign body reaction with local inflammation (e.g oedema, induration), And granuloma formation can result in a palpable, tender mess.

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54
Q

What are the two non-invasive breast cancers and the three invasive breast cancer?

A

Non-invasive: DCIS and Paget disease
Invasive: ductal carcinoma and lobular carcinoma and inflammatory breast cancer

characteristics laterrrr!!!!!

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55
Q

What are the two non-invasive breast cancers and the three invasive breast cancer?

A

Non-invasive: DCIS and Padget disease

Invasive: ductal carcinoma and lobular carcinoma and inflammatory breast cancer

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56
Q

Key features of DCIS (3)

A
  1. central necrosis
  2. precancerous lesion
  3. confined to ducts and lobules
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57
Q

Key features of paget disease (2)

A
  1. eczematous nipple lesion

2. extension of DCIS into ducts

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58
Q

Key characteristics of ductal carcinoma (2)

A
  1. most common type

2. nests and cords of cells

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59
Q

Key characteristics of lobular carcinoma (2)

A
  1. Small cells in single file

2. Mammary stroma invasion

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60
Q

Key characteristics of inflammatory breast cancer (2)

A
  1. peau d’orange

2. Dermal lymphatic invasion

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61
Q

Mastitis
Most common in ——
presents …

A

most commonly occurs in lactating women.
Presents with pain, breast swelling, erythema.
Most patients also have systemic findings such as fever, malaise and leucocytosis.

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62
Q

Two types of surgical incision scars

A
  1. Hypertrophic scar: thick, raised, and pink fibrous tissue line that FOLLOW the original incision.
  2. Keloid scars: occurs due to disorganised collagen deposits. thick, rubbery appearance and extend outside the incision borders
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63
Q

How can Turner’s syndrome (45, XO) patient get pregnant/method?
After checking renal cardiac and thyroid examinations.

A

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%)

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64
Q

How to restore fertility in women with hyperprolactinaemia

A

Bromocriptine is a dopamine receptor agonist that inhibits pituitary prolactin secretion

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65
Q

how to achieve fertility in women with ovulatory failure who are normogonadotropic, normoprolactinemic, euthyroid ????

A

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

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66
Q

How to stimulate ovulation in women who have hypothalamic GnRH secretion ? (hypogonadotropic, hypogonadal anovulation)

A

Pulsatile GnRH infusion can stimulate ovulation.

pituitary and ovarian function must be intact for this method to work

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67
Q

How can Turner’s syndrome (45, XO) patient get pregnant/method?
After checking renal cardiac and thyroid examinations.

A

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

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68
Q

how to achieve fertility in women with ovulatory failure who are normogonadotropic, normoprolactinemic, euthyroid ????

A

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

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69
Q

How to stimulate ovulation in women who have hypothalamic GnRH secretion ? (hypogonadotropic, hypogonadal anovulation)

A

Pulsatile GnRH infusion can stimulate ovulation

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70
Q

What can hCG therapy do?

A

trigger the ovulatory cascade in an oocyte donor when her follicles are deemed mature.

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71
Q

turner syndrome characteristics 10 points

A
  1. Narrow, high arched palate
  2. low hairline
  3. webbed neck
  4. broad chest with widely spread nipples
  5. cubitus valgus
  6. short stature
  7. coarctation of aorta
  8. bicuspid aortic valve
  9. horseshoe kidney
  10. streak ovaries, amenorrhea and infertility
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72
Q

How to stimulate ovulation in women who have hypothalamic GnRH secretion ? (hypogonadotropic, hypogonadal anovulation)

A

Pulsatile GnRH infusion can stimulate ovulation

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73
Q

what is karyotype of turners syndrome + mechanism

A

45, XO

loss of paternal chromosome X

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74
Q

Congenital adrenal hyperplasia (adrenogenital syndrome)

what is it and MOST COMMON TYPE?

A

-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)

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75
Q

Androgen insensitivity syndrome
defect?
typical karyotype ?
appears?

A

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

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76
Q

Edward syndrome cause and presentation

A

trisomy 18, caused by meiotic nondisjunction. they have multiple anomalies, including cardiac defects, clenched fists, rocker bottom feet, omphalocele, and low set ears

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77
Q

cri du chat cause and presentation

A

due to de novo partial deletion of the short arm of chromosome 5 (5p-)
typically have round face, catlike cry, and microcephaly.

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78
Q

Down syndrome causes (2) + presentation

A

1- meiotic nondisjuntion
2- robertsonian translocation

flat face, oblique palpebral fissures, and epicanthal folds.

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79
Q

what is the most common cardiac anomaly in down syndrome

A

atrioventricular defects

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80
Q

how does turner syndrome manifest in neonate

A

1- lymphedema (swelling)
2- cystic hydromas (neck)
short stature, primary amenorrhea, aortic anomalies

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81
Q

What is an imperforate hymen

A

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.

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82
Q

how does a patient with imperforate hymen present?

A

-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.

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83
Q

imperforate hymen examination shows :

A

vaginal bulge and/or mass palpated anterior to the rectum

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84
Q

Asherman syndrome leads to what?

A

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)

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85
Q

What is endometriosis

A

The presence of endometrial glands and stroma outside the uterus.

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86
Q

Can endometriosis cause amenorrhea

A

NO only severe dysmenorrhea with lower abdominal cramps that begin 1-2 days before menses.

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87
Q

What is it common site of endometrial implants

A

pouch of Douglas which presents as painful defecations, dysparunia, amd palpable nodularity on rectovaginal examination

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88
Q

What is the most common cause of primary amenorrhea

A

turner syndrome

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89
Q

Can Turner syndrome patient develop secondary sexual characteristics

A

No

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90
Q

What is Kallmann syndrome and how does it present

A

Impaired synthesis of gonadotropin- releasing hormone by the hypothalamus.
presents with:
1- primary amenorrhea
2- absent secondary sexual characteristics.
3- olfactory sensory defect

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91
Q

in what phase is progesterone secreted (menstrual period)

A

luteal phase

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92
Q

fxn of progesterone in period

A

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

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93
Q

taking exogenous progesterone for 10 days , do what?

A

matures the endometrial lining

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94
Q

explain menstrual flow

A

-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

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95
Q

what is dysplasia

A

abnormal growth of cells, tissues, or organs

e.g transformation zone of the cervix

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96
Q

what is granulation

A

process of scar formation that involves deposition of connective tissue and angiogenesis

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97
Q

why women with Asherman syndrome dont bleed (no progesterone withdrawal bleeding)

A

because the endometrium is essentially replaces with scar tissue

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98
Q

what is hyperplasia

what is hypertrophy

A
  • 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
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99
Q

in what dx is uterine hypertrophy seen?

A

ADENOMYOSIS

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100
Q

What is the primary hormone responsible for stimulating the endometrium (to be suitable for implantation)

A

progesterone

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101
Q

what is fibroadenoma ?

age?

A

MOST COMMON benign tumor of the breast

-YOUNG WOMEN 15-35

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102
Q

describe fibroadenomas

A

nodules that are well-demarcated,painless, mobile, and spherical, 1-10 cm in size.

they can also occur as multiple and/or bilateral lesions

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103
Q

how young vs old women discover fibroadenoma

A

young: usually discovered as palpable mass by pt/physician
old: incidentally or mammography

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104
Q

when do fibroadenomas increase/decrease in size?

A 
increase:
1- pregnancy
2- lactation 
3- with estrogen therapy 
decrease: 
1- after menopause
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105
Q

histology of fibroadenomas

A

benign-appearing cellular or myxoid stroma!!!!!
that encircles epithelium-lined glandular and cystic spaces.

-well defined border
but may compress/distort surronding glandular epithelium

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106
Q

what happens to fibroadenomas as women age

A

epithelium atrophies and the stroma becomes more hyalinized

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107
Q

what is DCIS

A

malignant clonal cell proliferation CONTAINED by the surrounding ductal basement membrane.

108
Q

what layer is preserved in DCIS

A

-the basal (myoepithelial) layer of the duct is preserved and uninvolved

109
Q

characteristics of mammary duct ectasia

A
  • ductal DILATATION
  • inspissated breast secretions
  • chronic granulomatous inflammation in the periductal and interstitial areas
110
Q

medullary carcinoma of the breast

A

characterized by:

  • solid sheets of vesicular, pleomorphic, mitotically active cells
  • significant lymphoplasmacytic infilitrate (around and within) the tumor.
  • pushing, noninfiltrating border
111
Q

what is paget disease OF THE NIPPLE ?

physical exam?

A 
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
112
Q

what is sclerosing adenosis ?

A

COMMON FINDING IN: fibrocystic changes
characterized by:
central acinar proliferation and compression with surrounding fibrotic tissue and peripheral ductal dilation

113
Q

risk factors of epithelial ovarian cancer

A 
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
114
Q

protective factors of epithelial ovarian cancer

A 
1-Combined OCP**
2- multiparity **
3- breastfeeding**
4- salpingo-oophorectomy 
sos: they decrease the frequency of ovulation, i.e less trauma and repair
115
Q
  • abdominal distension
  • ascites
  • pleural effusion
  • bowel obstruction
  • decreased appetite
  • weight loss
  • ovarian mass
A

Epithelial ovarian cancer (EOC)

116
Q

ovarian cancer marker

is it sensitive/ specific ?

A

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)

117
Q

why nulliparity is a risk factor for ovarian cancer

A

it means repeated ovullation

118
Q

why nulliparity or infertility lead to ovarian cancer?

A

they inflicit minor trauma to the ovarian surface, therefore rendering the epithelia susceptible to transformation

119
Q

to what cancers is HPV infection linked?

A

cervical
vaginal
vulvar
NOT OVARIAN

120
Q

long term antioxidant supplementation (VITAMIN C) and cancer risk

A

antioxidant neutralize reactive oxygen species ROS and free radicals, so they decrease damage to cells.
answer: not proven yet :)

121
Q 
GENITAL DEVELOPMENT NOTES 
remember: 
<6 wks 2 pairs of genital ducts: 
1- paramesonephric (mullerian) 
2- mesonephric (wolfian)
A

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
122
Q

mullerian aplasia
aka vaginal agenesis
or Mayer-Rokitansky-Kuster-Hauser (MRKH) syndrome

SOSOSOSOS

A

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)
123
Q

all females with mullerian defect should check what

A 
renal ultrasound (50% have coexisting urologic anomaly) 
e.g unilateral renal agenesis !!
124
Q

what deficiency is most common in congenital adrenal hyperplasia ?

A

21- hydroxylase deficiency

125
Q

how does late onset 21- hydroxylase deficiency present?

A
  • hirusutism
  • oligomenorrhea
  • acne
126
Q 
Klinefelter syndrome (47,XXY) characteristics 
-affects males
A
  • tall stature (long legs)
  • poorly developed secondary sexual characteristics (no facial/body hair)
  • atrophic testes
  • infertility
  • intellectual disability
  • gynecomastia
127
Q

47, XXX characteristics

A

-tall stature
- slightly decreased IQ scores
- normal physical features
(including sexual development)

128
Q

female sexual interest/arousal disorder.

diagnosis?

A
  • 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
129
Q

female sexual interest/arousal disorder.

what is it?

A 
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

130
Q

SSRI and Noreepinephrine-dopamine reuptake inhibitor

effect on sexual activity

A

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

131
Q

female orgasmic disorder definition

A

-marked delay in, decreased frequency, and intensity of orgasms

or
-absence of orgasm

132
Q

genitopelvic pain/penetration disorder

A

involves recurrent difficulties with pain or fear of pain with vaginal intercourse or penetration attempts

133
Q

how menopause affects sexual activity?

hint: estrogen

A

peri- and post-menopausal (declining levels of estrogen) may be associated with decreased sexual interest..
accompanies by:
-decreased lubrication !!

134
Q

clinical feautures of gonococcal cervicitis

A
  • purulent or mucopurulent discharge
  • friable cervix with easy bleeding
    (e. g. intermenstrual or postcoital bleeding)

classically ASYMPTOMATIC

135
Q

diagnosis of gonococcal cervicitis / testing

A

Nucleic acid amplification testing !!!!!

136
Q

treatment of gonococcal cervicitis

A

3rd generation cephalosporins
PLUS
azithromycin or doxycycline

137
Q

untreated; cervicitis :

bacterias and complications

A

N. gonn and Chlam trach
ascends to the upper genital tract causing PID
leading to ectopic pregnancy or infertility

138
Q

how PID cause infertility

sos

A

results in tubal factor infertility d/t scarring of the fallopian tube!!!

139
Q

are gonococcal and chlamydial infections RF to cervical cancer?

A

no

140
Q

effect of ocp on ovarian cancer

A

decreased risk

141
Q

is cervicitis RF for ovarian ca

A

no

142
Q

EFFECT OF OBESITY/ ESTROGEN ON ENDOMETRIAL HYPERPLASIA

A

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 :)) !!

143
Q

endometrial sampling showing:

  • coiled glands filled with carbohydrate-rich mucus
  • edematous stroma
  • tortuous spiral arteries

what phase of the period?

A 
secretory phase (b/w ovulation and menses) 
days:15-28
144
Q

secretory phase endometrial biopsy

A

—> 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)

145
Q

uterine endometrium anatomy revision

A

upper layer: stratum functionale

consists of lamina propria (studded with tubular glands), spiral arteries and dilated capillaries.

146
Q

what marks the beginning of the proliferative phase and when does it end?

A

BEGINS: first day of menses
ENDS: with ovulation

147
Q

what is the function of estrogen in the proliferative phase?

A

stimulates proliferation of the stratum functionale

148
Q

how does the endometrium looks during proliferative phase?

A

-non branching, non budding, uniform GLANDS.

evenly distributed throughout a uniform STROMA

149
Q

midprolifertaive phase biopsy of the endometrium

A
  • 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.
150
Q

endometrial biopsy at ovulation

A

shows late proliferative endometrium with coiled glands and occasional cytoplasmic vacuoles in the glandular epithelium

151
Q
  • painful urination
  • urinary frequency/urgency
  • suprapubic tenderness
  • NO FEVER,FLANKPAIN, COSTOVERTEBRAL ANGLE TENDERNESS
A

ACUTE CYSTITIS

152
Q

how CYSTITIS arise?

A

fecal organisms!!!!! gain access to urethral meatus and ascend to bladder

153
Q

most common causes(bacterias) of cystitis

A
  • E.coli 70% -gram -ve coliform bacteria
  • other Enterobateriaceae (less common)
  • Klebsiella pneumonia
  • Proteus mirabilis
154
Q

why do women develop UTI more common (2)

A

1- proximity of the anus and vaginal introitus

2-short length of female urethra

155
Q

most common cause (bacteria) of vulvovaginitis

A

Candida albicans

156
Q
  • vaginal discharge
  • burning
  • PRURITIS
A

vulvovaginitis

157
Q

STDs in symptomatic women

sos this symptom

A

SIGNIFICANT mucopurulent vaginal discharge

158
Q
  • asymptomatic
    or
    -thin whitish vaginal discharge
    -FISHY vaginal odor
A

Bacterial vaginosis

159
Q

what is the normal vaginal flora (e.g) ad in what dx it is replaced and with what?

A

normal (e..g Lactobacillus)

is replaced by facultative anaerobes (e.g Gardnerella vaginalis) in bacterial vaginosis

160
Q

what colonizes the genital and GI tract? so rarely cause infections

A

group B streptococcus

161
Q

early neonatal sepsis cause

A

group B streptococcus passed to infants during vaginal birth

162
Q

what women are more susceptible to get UTI by uncommon UTI organisms:
1- Pseudomonas aeruginosa
2- Staphylococcus
although E.coli is still more common !!!

A

1-recently received antibiotics

2-have been hospitalised

163
Q

enteric pathogen

A

E.coli

164
Q

mos common cause of genital herpes

A

HSV-2 !!

165
Q

-cluster of PAINFUL vesicles, pustules and/or ulcers on:
labia, penis, buttocks, or THIGH
+/- systemic symptoms in primary infection
(fever)

A

genital herpes

166
Q

tx of genital herpes

A

Acyclovir,
famciclovir, or
valacyclovir

167
Q
  • systemic symptoms (fever, myalgia)
  • inguinal lymphodenopathy !!!
  • itchy, painful, vesicular genital rash
A

PRIMARY genital herpes !!

168
Q

what is the course of the characteristic rash on the genitalia or buttocks

A

STAGES

vesicular—> ulcers —> crusting !!!

169
Q

following infection, where does HSV remain dormant

A

sacral dorsal root ganglia

170
Q

which is stronger primary or recurrent HSV

A

recurrence is more localized and less severe due to humoral immunity

171
Q

when is HSV more contagious

A

during RECURRENCE

172
Q

do contraception preven HSV spread

A

YES

173
Q

What is a neurological manifestation of lyme disease

A

Facial nerve palsy

174
Q

what causes lyme diseases

A

sphirocete Borrelia burgdorferi

or HSV-1

175
Q

HSV-1

oral vs genital

A

ORAL MORE

176
Q

-fatigue
-anorexia
-headache
-occasional fever
WITHOUT a vesicular rash

A

Lyme disease

177
Q

untreated syphilis —> tertiary neuro manifestations ?

A

infects the dorsal roots of the spinal column and lead to tertiary neurosyphilis characterized bt:
1- tabes dorsalis (locomotor ataxia)
2- general paresis

178
Q

how does primary syphilis present

A

SINGLE painless genital lesion (CHANCRE) after intital infection with Treponema pallidum sphirocete)

179
Q

Varicella zoster virus effect on neuro

A

ALSO (like syphilis) invades the dorsal root sensory ganglia.
and reactivation causes herpes zoster (e.g shingles)

180
Q

neurological complication of shingles

A

Postherpetic neuralgia (persistent pain after resolution of lesions)

181
Q

typical presentation of herpes zoster is

SOS

A

PAINFUL vesicular rash in a dermatomal distribution

WITHOUT systemic involvement

182
Q 
HPV human papillomavirus 
what is it?
what type of cells it infects?
what cancers?
skin manifestation?
A
  • oncogenic double-stranded DNA virus
  • infects EXCLUSIVELY epithelial cells.
  • predispose cervical, vulvar carcinoma
  • WARTS
183
Q

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)

A 
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
184
Q

association for bacterial vaginosis

A
  • smoking
  • sexual activity
  • vaginal douching
185
Q

why vaginal pH increases in bacterial vaginosis !!!!

A

decreased lactobacilli colonization

186
Q

what causes fishy smell in bacterial vaginosis?

A

anaerobic bacterias (e.g gardnerella vaginalis) generates malodouros amines
amines lead to:
1- GRAYISH WHITE
2- FISHY SMELLING

187
Q

what are clue cells !!

A

clue cells : SQUAMOUS epithelial cells with adherent bacteria.

shown in Wet mount microscopy of bacteria in bacterial vaginosis shows

188
Q

what is positive whiff test and in what disease

A

in bacterial vaginosis

-application of potassium hydroxide to the discharge produces an amine odor ;)

189
Q

wet mount microscopy of normal vaginal discharge (physiologic leukorrhea) shows:

note: it is not malodourous

A

epithelial cells and rare leukocytes

190
Q

-cervical erythema
-friability
-purulent cervical discharge
what type of bacteria?

A

N. gonorrhea cervicitis

gram -ve intracellular diplococci

191
Q

underlying mechanism of turner syndrome

A

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)

192
Q

what gene is missing in turner syndrome? and its fxn?

A

SHOX gene!!!! which promotes long bone growth , thus pts have short stature!!!

193
Q

meiotic nondisjunction occurs in what syndromes?

A

Turner syndrome
Klinefellter syndrome
trisomies 13,18,21

194
Q

what is a balanced translocation?

A

clinically silent as there is no excess or shortage of genetic material.

195
Q

what is the risk of a balanced translocation?

A

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

196
Q

what is a frameshift mutation

A

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)

197
Q

give 3 examples of dx’s with trinucleotide repeat expansion

A 
fragile x syndrome (CGG repeats)
myotonic dystrophy (CTG repeats)
Huntington disease (CAG repeats)
198
Q

what is uniparental disomy?

and examples

A

individual inherits 2 copies of a chromosome from one parent only.
1- angelman syndrome
2- prader-willi syndrome
(on chromosome 15 both)

199
Q

turner syndrome 3 types of karyotype

A

45,X complete monosomy
45,X/46,XX mosaicism
46,XX w/ partial deletion of one x chromosome

200
Q

proteins in gap junction + fxn

A

Connexins

-intracellular communication

201
Q

proteins in tight junction + fxn

A

Claudins, occludin

-paracellular barrier (to water and solute)

202
Q

proteins in adherens junction + fxn

A

Cadherins

-cellular anchor (similar to desmosomes and hemidesmosomes)

203
Q

proteins in desmosomes + fxn

A

Cadherins
(e.g desmogleins, desmoplakin)
-cellular anchor
(similar to adherens junction and hemidesmosomes)

204
Q

proteins in hemidesmosomes + fxn

A

Integrins

-cellular anchor (similar to desmosomes and adherens junction)

205
Q

what type of cell junction is important during labor?

A

gap junction

206
Q

effect of estrogen on cell junction (during labor)

A

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.

207
Q

effect of estrogen on oxytocin receptor (during labor)

A

oxytoocin receptors are uterotonic receptors. which mediate calcium transport through ligand-activated calcium channels

208
Q

2 requirements to have a coordinated, synchronous labor contractions

A

1- increase in gap junction density

2- uterotonic (oxytocin) receptors

209
Q

both adherens junctions and desmosomes are composed of cadherins
what are the different cytoplasmic anchors?

A
  • adherens junction: actin filament

- desmosomes: intermediate filament

210
Q

Autoantibodies agains desmoglein

(a cadheren protein for desmosome) found in what disease

A

pemphigus vulgaris

211
Q

what are fenestrae?

A

gaps b/w endothelial cells that allow for paracellular transport.

212
Q

new-onset hypertension
proteinuria
end-organ dysfuction
at >/= 20 wks gestation

+ pathophysiology

A

preeclampsia

Swollen fenestrae in renal glomerular capillary endothelial cells

213
Q

Autoantibodies against hemidesmosomes leads to: 2:

A

1- bullous pemphigoid

2- pemphigoid gestationis

214
Q

how tight junctions are connected to food poisoning?

A

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

215
Q
  • lower abdominal pain (pelvic cramping)
  • vaginal bleeding
  • positive pregnancy test (e.g detectable b-hCG) !!
  • palpable adnexal mass !!!
A

ECTOPIC PREGANNCY

216
Q

locations of ectopic pregnancy

and whats the most common

A 
1- tubal (most common 90 %) 
in the fallopian tube!!
2- cornual/interstitial
3- ovarian 
4- abdominal 
5- cervical
217
Q

give example of tubal pathology that often cause ectopic pregnancy (2)

A

1- PID

2- prior pelvic surgery

218
Q

how tubal ectopic pregnancy leads to the classic symptoms of pelvic cramping! and vaginal bleeding! (e.g spotting)?

A

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

219
Q

hydatidiform mole typical presentation

A

-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)

220
Q

are fibroids associated with b-hCG?

A

no

221
Q

uterine fibroids locations

A 
1- intracavitary 
2- submucosal
3- intramural
4-subserosal
5- pedunculated 
(in order from inside to outside)
222
Q

what is endometrioma

A

ectopic endometrial tissue in the ovary

*can cause adnexal mass and vaginal bleeding if ruptured

223
Q

*dysmenorrhea and endometriosis symptoms (dyspareunia, dyschezia)
*adnexal mass
+/- vaginal bleeding

A

endometrioma +/- rupture

224
Q

what is mature teratoma

A

ovarian mass composed of
ectoderm
endoderm
mesoderm

225
Q

pt with a mature teratoma are at risk of what?

A

ovarian torsion

226
Q
  • pelvic pain
  • palpable adnexal mass
  • SUDDEN and UNILATERAL pain
  • uncommon vaginal bleeding
A

OVARIAN TORSION

227
Q

task

sos

A

google how candida looks in wet microscopy :)

and clue cells in BV
and trichomonias

228
Q

what can cause an imbalance in the normal vaginal flora
i.e excessive candida (usually a bit) ?
and list some risk factors

A

—> 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) !!!
229
Q

how is candidal vulvovaginitis diagnosed?

A

wet mount microscopy

reveals pseudohyphae with budding yeast and true hyphae

230
Q

MoA of azole (antifungake med)

FLUCONAZOLE?

A

DECREASE ergosterol synthesis

and dirsupt fungal cellular membrane formation

231
Q

tx of herpes simplex virus

A

acyclovir

232
Q

how is herpes simplex virus visualized

A 
cervical CYTOLOGY (not wet mount microscopy) 
shows multinucleated giant cells
233
Q

can HSV cause cervicitis?

A

RARELY

234
Q

what abx is azithromycin

A

macrolide

235
Q

what abx is ceftriaxone

A

3rd gen cephalosporins

236
Q

why C. trachomatis cannot be easily visualized in microscopy?

A

d/t its unusal peptidoglycan cell wall

237
Q

pt with INTERMITTENT leakage of urine likely has

+leakage during valsalva maneuver

A

Stress urinary incontinence

SUI

238
Q

how pelvic floor muscles maintain continence in women? !!

A
  • 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
239
Q

how the pelvic floor muscles become weak ? !!!

A

chronically increased intraabdominal pressure
-obesity
-chronic cough from COPD !!!!!
ALSO
-prior pregnancies!! (incl cesarean)
it increase the laxity of pelvic floor muscles and CT.

240
Q

stress urinary incontinence tx

A

pelvic floor muscles (i.e kegel) exercises and pessary placement (help support and maintain normal pelvic anatomy)

241
Q

most common cause of vesico-vaginal fistula

A

bladder injury from surgical or obstetric complications (e.g operative vaginal delivery)

242
Q
  • CONTINUOUS urinary dribbling

* leakage of urine from VAGINA (not urethra)

A

vesico-vaginal fistula

243
Q

bladder

sympathetic vs parasympathetic

A

sympathetic:
- promotes urine storage &continence (by increasing urethral sphincter tone)
parasympathetic:
- stimulates detrusor muscle contraction and micturition

244
Q 
sos 
fill: 
cholesterol —> androgens —> estrogen 
in what ovary cell types these steps take place 
or
note:

cholesterol —> progesterone

A

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
245
Q

what is the predominant estrogen in the human body

A

estradiol (derived from ANDROGENS)

246
Q

what is the role of theca externa ?

is it involved in steroidgenisis?

A

NO,
composed of a layer of SM and fibroblast cells.
so connective tissue support structure for the follicle :)

247
Q

female oocyte timeline

  • embryogenesis:
  • ovulation:
  • fertilization:
A
  • embryogenesis: formed here and remain arrested in prophase 1 until ovulation.
  • ovulation: single oocyte completes meiosis I
  • fertilization: meiosis II occurs
248
Q

where are leydig cells found?

analogues to what in the other gender?

A

MALE testes only
analouges to theca interna cells of the ovarian follicle.
i.e stimulated by LH to secrete testosterone

249
Q

HPV STRAINS PRESENTATION
1-4
6,11
16,18

A

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

250
Q

most common type of cervical cancer

A

SCC

arises from teh squamocolumnar junction of the endocervix

251
Q

what is CIN ?
dysplasia d/t —
!!!!!!

A

cervical intraeoithelial neoplasia is CARCINOMA IN SITU , precedes SCC.
dysplasia d/t HPV

252
Q

what women are at risk of invasive cervical cancer ?

A
  • persistent HPV infection

- Untreated high-grade CIN

253
Q

How high risk strains of HPV cause malignancy

A

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)
254
Q

Cervical cancer RF are related to what RF?

A

the risk of acquiring HPV infection

  • hx of multiple partners
  • lack of barrier contraceptive (e.g condom) use !!!
255
Q

alcohol increases risk of what cancer

A

Liver

Breast

256
Q

Nulliparity, early menarche, obesity increases risk of what cancer
and why

A 
endometrial cancer 
(these factors are associated with increased estrogen stimulation of the endometrium )
257
Q

DOUCHING is a risk factor of

A

Bacterial vaginosis

-disrupts the vaginal ecosystem resulting in overgrowth of gardnerella vaginalis

258
Q

LYMPH NODE DRAINAGE of the female reproductive system

  • Uterus
  • Cervix
  • Vagina
  • Vulva
  • Ovaries
A
  • 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)
259
Q

most common type of vulvar cancer

A

SCC

260
Q
  • ulcerative lesion or

- plaque on the LABIA

A

vulvar cancer !!

261
Q

RFs of vuulvar cancer (3)

A

1- chronic HPV infection
2- prior vulvar lichen sclerosus
3- tobacco use

262
Q

what is sentinel lymph node biobsy? !!

A

first lymph nodes to drain th PRIMARY tumor site

263
Q

what is the lymph drainage of the lower extremities, buttocks and external genitalia) ?

A

lymph from:

  • uterine corpus
  • inguinal nodes

these drain to the external iliac nodes

then, external + internal drain to common

264
Q

lymph drainage of the bladder, uterus, and cervix

A 
obturator nodes
(located in the obturator fossa medial to the external iliac vessels.
265
Q 
pelvic lymph node groups 
1- obturator
2- external iliac
3- internal iliac 
drain all together:
A

pelvis
lower extremities
lower abdominal wall

266
Q

where does the common iliac drain to

A

paraaoric lymph nodes

267
Q

lymph drainage of anal canal amd rectum

A

presacral lymph nodes

FEMALE reproductive (6 decks)

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