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Reproductive > Lec 6 Benign Ovary > Flashcards

Lec 6 Benign Ovary Flashcards

1
Q

What are the 3 functions of ovary?

A
  • house gametes
  • secrete estrogen, progesterone, testosterone
  • produce egg during ovulation in response to hormonal stimulation
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2
Q

What are disorders of sexual differentiation?

A

discrepancy between external genitalia and internal

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3
Q

What are the 3 categories of disorders of sexual differentiation?

A
  • 46 XX [female pseudohermaphrodite]
  • 46, XY [male psueodhermaphrodite]
  • mixed sex chromosome [true hermaphrodite or gonadal dysngenesis]
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4
Q

What are characteristics of person with 46 XX DSD [= 46 XX with virilization]?

A
  • ovaries and normal uterus and fallopian tubes
  • external genitalia look ambiguous or male
  • labia fuse and clitoris appears enlarged like a penis
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5
Q

What are 3 causes of 46 XX DSD [virilization]?

A
  • congenital adrenal hyperplasia
  • gestational hyperandrogenism
  • testicular and ovotesticular DSD
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6
Q

What is most common cause of sexual ambiguity of newborn?

A

congenital adrenal hyperplasia

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7
Q

What is the internal duct system in females?

A

paramesonephric ducts –> give rise to uterus, fallopian tubes, upper vagina

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8
Q

What is the internal duct system in males?

A

mesonephric ducts –> give rise to vas deferens, epididymis, seminal vesicles

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9
Q

How does 21-alpha-hydroxylase deficiency present?

A
  • high 17-hydroxyprogesteron

- can have salt wasting –> hyponatremia, hyperkalemia, hypotension

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10
Q

What are some causes of gestational hyperandrogenism?

A
  • male hormones [testosterone or synthetic progestational agents] taken by mother during pregnancy
  • male hormone-producing tumor in mother
  • placental aromatase deficiency [normally converts testosterone to estradiol]
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11
Q

What is 46 XX ovotesticular DSD?

A

virilization with mixed ovarian and testicular tissue = either ovotestis or ovary and testis

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12
Q

What happens to development in absence of testosterone?

A

system programmed to develop internally and externally as a phenotypic female

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13
Q

What is action of MIF [mullerian inhibiting factor]?

A

stimulates development of male [wolffian] duct system and regression of female

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14
Q

What are 4 causes of 46 XY DSD?

A
  • congenital adrenal hyperplasia
  • abnormal testicular activity
  • abnormal androgen synthesis
  • abnormal response to androgen
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15
Q

What is presentation of 46 XY DSD?

A
  • external genitals incompletely formed, ambiguous, or clearly female
  • internally testes may be normal, malformed, or absent
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16
Q

What does serum conc of mullerian inhibiting substance tell you?

A

marks sertoli cell mass; it is normal when functional testicular tissue is present

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17
Q

What is effect of decreased MIS secretion/action early in development?

A

fully developed mullerian duct structures = gonadal dysgenesis or persistent mullerian duct syndrome

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18
Q

What is effect of decreased MIS secretion/action late in development?

A

partial regression of mullerian duct structure = testicular regression syndrome, vanishing testis syndrome, or congenital anorchia

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19
Q

What do low MIS levels in a 46, XY individual suggest?

A

gonadal dysgenesis = have femal external genitatlia, intact mullerian ducts, streak gonads

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20
Q

What is most common cause of abnormal androgen synthesis in 46 XY DSD?

A

17-beta-hydroxysteroid dehydrogenase type 3 deficiency –> low/normal serum testosterone, very high androstenedione

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21
Q

What happens in 5-alpha reductase type 2 deficiency?

A

autosomal recessive 46 XY with bilateral testes and normal testosterone but defect converting testosterone to more potent DHT

may have normal male genitalia or femal or ambiguous; the most changed to external male genitalia occurs in puberty with increased androgen production

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22
Q

What is the most common cause of 46 XY DSD?

A

androgen insensitivity syndrome –> normal testes and testosterone but receptors don’t function properly

get testicular feminization

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23
Q

What is the presentation of patients with androgen insensitivity syndrome?

A
  • have breasts
  • absent axillary and pubic hair
  • absent upper vagina/uterus/fallopian tubes/ovaries = has a blind vaginal pouch
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24
Q

What is mixed gonadal dysgenesis vs true hermaphroditism?

A

mixed gonadal dysgenesis = 1/3 raised as males; have ambiguous external genitalia and persistent mullerian duct regardless of adjacent gonad

true hermaphroditism = 3/4 rales as males; internal duct development corresponds to adjacent gonad

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25
Q

What is turner syndrome?

A

45XO; phenotypically female but have physical abnormalities –> webbed neck, edema on dorsum of hands/feet

internally have streak [nonfunction/fibrous] gonads

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26
Q

How does turner syndrome present?

A

short stature, streak ovary, amenorrhea, low hairline, shield chest, infantile uterus

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27
Q

What is klinefelter?

A

47 XXY due to nondisjunction of sex chromosomes in either parent

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28
Q

What is most common cause of primary amenorrhea?

A

turner syndrome

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29
Q

What is most commone cause of congenital abnormality causing primary hypogonadism?

A

klinefelter syndrome

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30
Q

How common in klinefeleter?

A

1 in 850

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31
Q

What is presentation of klinefelter?

A

small, firm testes with low sperm count, infertility, high FHS/LH
low testosterone
eunuchoid body shape, tll long extremities, gynecomastia, female hair distribution

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32
Q

What is mixed gonadal dysgenesis?

A

45X/46XY or 46 XY
phenotypically ambiguous
have persistent mullerian duct regardless of adjacent gonad [unlike true hermaphrodie]
- have one streak gonad and a contralateral abnormal testit
- sterile

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33
Q

What is appearance of ovotesticular DSD?

A

can be phenotypically ambiguous or male or female
genotype 46XX or 46XY or mosaic
by definition have both ovarian and testicular tissue [separate ovary and testis or combined ovotestis]

internal duct system corresponds to the gonad [vs in gonadal dysgenesis fallopian tube adjacent to testis]

34
Q

Is uterus present in true hermaphrodite?

A

yes

35
Q

What percent of true hermaphrodites are raised males vs females?

A

3/4 male

1/4 female

36
Q

Are pts with ovotesticular DSD [true hermaphroditism] fertile?

A

some are fertile

37
Q

What do the mesonephric ducts give rise to?

A

vas deferens
epididymis
seminal vesicles

38
Q

What do the external genitalia and urethra develop fomr?

A

urogenital sinus and genital tuberlce

39
Q

What does the urogenital sinus give rise to?

A

boys: prostate and prostatic urethra
girls: urethra and lower portion of vagina

40
Q

What does the genital tubercle become?

A

boys: glans penis
girls: clitoris

41
Q

What do you urogenital swellings become?

A

scrotum or labia majora

42
Q

WHat do the genital folds become?

A

labia minora or fuse to form male urethra and shaft of penis

43
Q

What is necessary for ovarian development?

A

all 46XX chromosomes –> 45XO turners will have atretic ovaries = fibrous non-functional

44
Q

What is required for differentiation of indifferent gonad into testis?

A

testis determining factor [TDF] which is located in SRY region of Y chromosome

45
Q

What happens if no TDF gene?

A

gonadal dysgenesis

46
Q

Where does mullerian inhibiting factor come from? actions?

A

synthesized by sertoli cells and causes ipsilateral regression of mullerian ducts by week 8

also plays a role in testicular descent

47
Q

What stimulates wolffian [mesonephric] duct growth?

A

testosterone from leydig cells

48
Q

What develops in absence of MIF?

A

fallopian tubes, uterus, upper vagina

49
Q

What happens if low levels of MAF?

A

partial development of wolffian ducts and partial regression of para-mesonephric ducts

50
Q

When do the testis begin secreting testosterone?

A

around 8 weeks

51
Q

Why is it important to have 5a reductase?

A

converts testosterone to DHT = more potent active hormone

causes ambiguous genitalia until puberty with normal internal genitalia

52
Q

What are the 3 majors types of non-neoplastic ovarian cysts?

A
  • functional [follicular] cysts
  • endometriotic cysts
  • polycystic ovarian syndrome [PCOS]
53
Q

What is best way to assess a newly discovered mass?

A

ultrasound

–> thick septations and solid components in cyst are suspicious for malignancy

54
Q

How long does it take for physiologic ovarian cysts to regress?

A

6-10 weeks

55
Q

What is an ovarian cyst?

A

collection of fluid surrounded by thing wall within an ovary

if smaller than 2 cm = cystic follicle = harmless

56
Q

What is a follicular cyst vs corpus luteum cyst?

A

follicular = follicle fails to release egg; fluid not reabsorbed and cyst formed

corpus luteum = after eggr released from follicle

57
Q

What is size of functional cyst?

A

> 2cm

58
Q

Who gets functional cyst?

A

women of reproductive age

59
Q

What is clinical presentation of functional cyst?

A 
usually asymptomatic
sometimes
- pelvic pain
- abnormal uterine bleeding
- dyspareunia
60
Q

What lines follicular cyst internally?

A

follicle lining cells = granulosa and theca interna cells

61
Q

What is effect of oral contraceptive use on ovarian cysts?

A

decreases risk of developing cyst b/c prevent development of follicles

62
Q

What test should you check in woman with ovarian cyst and abnormal ultrasound or older age?

A

Ca-125 to look for cancer

63
Q

What blood tests should you order in woman with ovarian test?

A
  • Ca-125 for cancer
  • HCG for pregnancy
  • LH/FSH/estradiol/testosterone
64
Q

What is treatment for functional cysts?

A

regress spontaneously in 60 days; can accelerate by treatment with high dose oral contraceptives

65
Q

What is endometriosis?

A

cells from lining of uterus [endometrium] appeara and grow outside uterine cavity [commonly ovary]

66
Q

How common is endometriosis?

A

10-15% of reproductive age women

67
Q

What are symptoms of endometriosis?

A
  • pelvic pain, dysmenorrhea, low back pain, dyspareunia [painful intercourse], dysuria that is worse around menses

commonly causes infertility

68
Q

What is etiology of endometriosis?

A

may be genetic predisposition; estrogen implicated

69
Q

What is gross appearance of endometriotic cyst?

A

cyst containing turbid brown content = chocolate cysts

70
Q

What is histo appearance of endometriotic cyst?

A

lining composed of endometrial-like glands and stroma and hemorrhage

71
Q

How do you diagnose endometriotic cyst?

A
  • MRI or ultrasound

- surgery = gold standard but not covered by insurance

72
Q

What is treatment for endometriosis?

A

pain control, hormonal therapy

73
Q

How common is polycystic ovarian syndrome?

A

5-10% of reproductive age women

74
Q

What is finding on sonogram in PCOS?

A

string of pearls arrangement of cystic follicles and thick, sclerotic cortical rim

75
Q

What is the pathogenesis of PCOS?

A
  • release of excess LH by the anterior pituitary OR
  • high levels of blood insulin OR
  • reduced levels of sex hormone binding globulin –> excess free androgens

–> results in ovaries producing excess androgens, high LH:FSH ratio

76
Q

How is PCOS inherited?

A

autosomal dominant with high penetrance but variable expressivity

77
Q

What is the appearance of a polycystic ovary?

A

ovary with abnormally large number of developing eggs visible near surface = looks like many small cysts or a string of pearls
ovary covered by thick fibrotic overlying capsule

78
Q

What is presentation of PCOS?

A
  • oligomenorrhea or amenorrhea
  • infertility [lack of ovulation]
  • hyperandrogenemia –> hirsuitism and acne
  • metabolic syndrome: central obesity, insulin resistance
79
Q

What is primary dysmenorrhea?

A

prostaglandins produced in uterus at menses resulting in menstrual cramp

80
Q

What are sonographic feat of benign vs malignant cysts?

A

benign: single locule, thin septations, unilateral
malignant: complex cyst, can be bilateral, thick septations, may have ascites

81
Q

How do you diagnose endometriosis?

A

tissue biopsy

82
Q

Why is laparoscopy better than laparotomy?

A
  • shorter recovery
  • less pain
  • less blood loss
  • less overall cost compared to laparotomy
  • even large cysts can be removed

Reproductive (14 decks)

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