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Endo/Repro II Test 1 > 20. Puberty Disorders of Development > Flashcards

20. Puberty Disorders of Development Flashcards

1
Q

Menstrual cycle occurs with the maturation of what _______.

A

Hypothalamic - pituitary - ovarian axis

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2
Q

[Arcuate nucleus of the hypothalamus] => __________ => [AP] => ____________ => acts on ________.

A

[Arcuate nucleus of the hypothalamus] => GnRH => [AP] => LH/FSH => acts on theca cells/ granulosa cells .

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3
Q

FSH and LH are stored in what cells?

A

Gonadotrophs in the AP.

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4
Q

LH => _____ cells => releases _____

A
  • LH => theca cells => androgens (androstenedione and testosterone)
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5
Q

FSH => ______ cells => releases _____

A

FSH => granulosa cells => converts androgens to estrogens (estrone = E1 and estradiol = E2)

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6
Q

Phases of the NL Ovarian Cycle

-What phases of the endometrium do they respond to?-

A
  1. Follicular phase: [1st day of menstruation => preovulatory stage of LH surge]
    1. Corresponds to: menstrual and proliferative phase of endometrium
  2. Luteal phase: [preovulatory stage of LH surge => 1st day of menstruation]
    1. Corresponds to: secretory phase of the endometrium
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7
Q

Describe the Ovarian Cycle

A

[1st day of period => pre-ovulatory stage of the LH surge]

  1. If conception does NOT occur, levels of progesterone/estradiol decrease as the corpus luteum from the previous cycle regresses.
  2. Initiates increase in FSH to cause follicles to grow: => granulosa cells => increase estrogens (estron/estradiol) => Large # of large antral follicle grows :)
  3. As follicle grows, increase estrogen negatively feedbacks and tells AP to decrease FSH secretion => all but ONE of the developing follicles will stop growing and die off
  4. Follicle with most FSH receptors becomes the dominant follicle that will secrete estrogen.
  5. Increase estrogren from dominant follicle will become more responsive to pulsatile action of GnRH
  6. Estrogen from dominant follicle become a positive feedback => Increases the amount of FSH/LH (LH surge) release from hypothalamus 1-2 days before ovulation => meitotic maturation, ovulation and luteinization.
  7. Corpus luteum produces high [progesterone and estradiol]
  8. High progesterone and estradoil negatively feedback on LH/FSH, to return to baseline levels
  9. If ovulation does not occur (hCG does not increase), CL will regress.
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8
Q

_____ enhances the hypothalamic release of GnRH and induce the midcycle LH surge.

A

Estradiol

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9
Q

_____ have an inhibitory effect on GnRH release.

A

Gonadotropins

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10
Q

When are estradiol levels low and when do they begin to rise?

A
  • Low = early follicular development
  • Rise = 1 week before ovulation bc will cause LH surge
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11
Q

Course of estrogen: when does it peak, what occurs after and during luteal plase?

A
  • Estrogen peaks 1 day before LH surge.
    • After peak and before ovulation => marked fall
    • During luteal phase => estradiol rises to a max 5-7 days after ovulation d/t release from CL => returns to BL before menstruation.
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12
Q

Describe levels of progesterone during the ovarian cycle.

A
  • Follicular phase: ovary secretes SMALL amounts. The bulk of it mainly comes from peripheral conversion.
  • Before ovulation: Unruptured luteinzing graafian follicle begins to secrete increasing amounts of progresterone
  • CL: secretes progesterone, which reaches max 5-7 days AFTER ovulation and returns to BL before menstruation.
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13
Q

What is the outcome of a mature graafian follicle (made from primordial follicle) ?

A
  1. Innermost 3-4 layers of granulosa cells become cuboidal and form cumulus oophorus.
  2. Fluid filled antrum forms amount granulosa cells => enlarges and pushes primary oocyte to wall.
  3. Innermost layer of granulosa cells of cumulus oophorus become elongated and form corona radiata.
  4. Ruptures => releases ovum + corona radiata
  5. Luteinization produces corpus luteum.
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14
Q

How does the LH surge result in ovulation?

A
  1. Degenerates cells on the wall of the follicle => forming a stigma.
  2. BM of follicle then bulges through stigma => ruptures => oocyte is expelled => ovulation.
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15
Q

What happens to the follicle AFTER ovulation?

A
  • Granulosa cells under luteinization => luteinizing granulosa cells, theca cells, CT and capillaries => corpus leutum (lives 9-10 days).
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16
Q

What happens to the corpus luteum if pregnancy does NOT occur?

A

Menses happens and CL is replaced by avascular scar (corpus albicans)

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17
Q

Zones of the endometrium

A
  1. Outer portion = functionalis
    1. Contains spiral arteries and undergoes cyclic changes, sloughing off during menstruation
  2. Inner portion = basalis
    1. Contains basal arteries and stem cells to renew endometrium; remains unchanged
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18
Q

Phases of the Endometrial Cycle

*which is the only phase seen visually*

A
  1. Menstrual phase (sloughing) *****
  2. Proliferative/estrogenic phase (grows)
  3. Secretory/progestational phase
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19
Q

Endometrial lining of a post-menopausal women should be HOW thick?

A

Less than 4mm

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20
Q

Describe the menstrual phase of the endometrial cycle

A
  • Begins at Cycle Day 1 = first day of menstruation
    • Conception did not occur by day 23 => CL regresses and progesterone/estradoil decline.
    • Cycle day 1: Functionalis layer sloughs off and compression of basalis layer: disruption of endometrial glands, stroma, leukocytes infiltrate and RBC extravasation
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21
Q

What hormones stimulates the proliferative phase of the endometrial cycle?

A

Estrogen => increase length of spiral arteries and mitosis

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22
Q

What hormone stimulates the secretory phase of the endometrial cycle?

How are the glands, stroma and mitosis affected?

A
  • After ovulation, CL releases progesterone => + secretory phase (stimulates glandular cells to secrete mucus, glycogen and substances)
    • Glands= tortous
    • Stroma = edematous
    • Mitosis = rare
    • Endometrial lining reaches MAX thickness
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23
Q

When must conception occur by, otherwise CL will regress and endometrium will undergo involution?

A

Day 23

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24
Q

What occurs in the secretory phase that prepares the endometrium for menstrauation?

A
  1. Conception did not occur by 23 => endometrium undergoes involution
  2. 1 day before => spiral arteries are constrictioned => endometrium undergoes ischemia and necrosis
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25
Q

What is IMPORTANT in regulation menstruation and why?

A

Intact coagulation pathway because with NL hemostasis, injured vesses are repaired quicky.

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26
Q

What is responsible for causing atresia of all but 1 follicle during the follicular phase - leading to selection of the dominant follicle; what does the dominant follicle produce?

A
  • ↓ FSH levels progressively cause atresia of all but 1 follicle
  • The dominant follicle produces high levels of estradiol
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27
Q

Diagnosis of menopause is made by looking at levels of what?

A

↑ FSH: since ovary is no longer receptive to FSH, there is no negative feedback on the AP

Menopause = ↑ FSH bc no (-) feedback

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28
Q
  • What is the median age of menarche (onset of period)?
  • When when does it occur in respect to Thelarche?
A
  • 12.43 years
  • 2-3 AFTER thelarche (breast budding) at Tanner stage IV.
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29
Q

Define primary amernorrhea.

A
  • No menstruation by 13 y/o WITHOUT secondary sexual development.

OR

  • No menstruation by 15 y/o WITH secondary sexual characteristics
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30
Q

What is the length of most normal menstrual cycles during the first gynecologic year and how does this change as more cycles occur?

A
  • Often irregular in adolescents, most normal cycles range from 21-45 days
  • By the 3rd year after menarche => cycles are 21-35 days
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31
Q
  • What is the mean blood loss per menstrual period?
  • How much loss is associated with anemia
  • What is a normal and abnormal amount of pad changes per day?
A
  • Mean blood loss is 30cc; changing pads/tampons 3-6x per day
  • Anemia = >80cc; changing pad q 1-2 hrs is considered excessive
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32
Q

How does obesity vs. a malnourished adolescent affect the onset of puberty?

A
  • Obese children have earlier onset of puberty
  • Malnourished, chronically ill w/ weight loss will have later onset
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33
Q

What is the invariant mean weight an adolescent needs to be or above to start menarche?

A

48 kg (106 lbs.)

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34
Q

Low levels of gonadotropin and sex steroids BEFORE puberty are due to what?

A
  1. Low estradiol (-) feedbacks gondastat (relates gonadotropin release)
  2. CNS inhibit secretion of GnRH
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35
Q

What are the initial endocrine changes assoc. w/ puberty?

A
  1. Production of adrenal androgen/sex steroids (DHEA, DHEA-S, and androstenedione) production
  2. Differentiation of the zona reticularis of the adenal cortex
  3. ====> Growth of axillary and pubic hair (adrenarche or pubarche)
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36
Q

Once puberty begins, what changes do we see in GnRH release?

A

Loss of CNS inhibition of GnRH release => released in pulsatile manner

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37
Q

Which hormones are required for thelarche (breast development) vs. pubarche/andrenarche (pubic/axillary hair developement)?

A
  • Thelarche requires estrogen
  • Pubarche/adrenarche requires androgens
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38
Q

What is the 1st physical sign of puberty and what is common in first 6 months?

A
  • Thelarche = breast development
    • unilateral breast development “one boob is growing bigger than the other”
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39
Q

What 4 factors does mecharche require?

A
  1. [Pulsatile GnRH] from hypothalamus
  2. [FSH/LH] from AP
  3. [Estrogen and progesterone] from ovaries
  4. NL outflow tract
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40
Q

What are the stages of normal pubertal development from earliest to latest?

A

*** TAG ME ***

  1. Thelarche
  2. Adrenarche
  3. Peak Growth/height velocity
  4. Menarche
  5. Mature sexual hair and breasts

*** TAG ME ***

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41
Q

Briefly describe the 5 Tanner stages of breast development.

A

- Stage 1: preadolescent elevation of papilla only

- Stage 2: breast bud stage; small mound w/ enlargement of areolar region

- Stage 3: more enlargement of breast + areola w/o separation of their contours

- Stage 4: [secondary mound] = projection of areola and papilla

- Stage 5: mature stage; projection of papilla only, recession of areola to general contour of breast

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42
Q

Briefly describe the 5 Tanner stages of pubic hair development.

A

- Stage 1: NO pubic hair

- Stage 2: Sparse, lightly pigmented hair along labia

- Stage 3: hair spreads sparsely over jct. of pubes; hair is darker + coarser

- Stage 4: adult-type hair, there is no spread to medial thigh

- Stage 5: spread to medial thighs assuming inverted triangle pattern

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43
Q

What is precious puberty and who is it more common in?

A
  • Development of secondary sex characteristics at an age 2.5 SD earlier than expected age of puberty.
  • F
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44
Q

What are the 2 major subgroups of precocious puberty?

A
  1. Heterosexual precious puberty: development of OPPOSITE secondary sex characteristics –> virilizing neoplasms, CAH, exposure to exogenous androgens
  2. Isosexual: premature sexual maturation that is APPROPRIATE for the phenotype of the affected individual –> constituional/organic brain disease
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45
Q

What is congenital adrenal hyperplasia?

What type of precious puberty can it lead to?

And which type is less severe and occurs later, in adolescents?

A
  • CAH defect in 21-hydroxylase => make excessive androgens
  • Heterosexual precocious puberty
  • Types
    • Classical = most severe and causes birth of F w/ ambigous genitalia
    • Nonclassical (late onset adrenal hyperplasia) => premature pubarche and an adult disorder the resembles PCOS
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46
Q

Which test can be administered clinically to diagnose true isosexual precocious puberty; what are you looking for?

A
  • Give exogenous GnRH (stimulation test)
  • See if ↑ in LH levels consistent w/ older girls who are undergoing normal puberty
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47
Q

True isosexual precocity vs Pseudoisosexual is caused by what?

A
  • True = Premature activation of NL pubertal processes that involve HPO axis
  • Pseudo = Increased estrogen w/o activation of HPO axis
48
Q

If a CNS disorder is suspected to be the cause of true isosexual precocious (75% are idiopathic/ consitutional) puberty, what is used to diagnose?

A

MRI of head

49
Q

Treatment of true isosexual precocious puberty

What is the important of treating this condition?

A

GnRH agonist (leuprolide acetate) —> will suppress release of FSH and LH

  • Untreated = <50% of girls will not grow over 5’ feet tall.
50
Q

What 2 syndromes can cause pseudoisosexual precious puberty?

A
    1. McCune Albright syndrome (Polyostotic fibrous dysplasia)
    1. Peutz-Jeghers syndrome
51
Q

What is seen in McCune-Albright syndrome (Polyostotic fibrous dysplasia)?

A
  1. Multiple cystic bone defects
  2. Café au lait spots (face, neck, shoulder and back)
  3. Adrenal hypercortisolism
52
Q

What is seen in Peutz-Jeghers syndrome?

A
  1. Sex cord tumor that secretes estrogen
  2. Mucocutaneous pigmentation
  3. GI polyposis
53
Q

Puberty is considered delayed in what 4 situations?

A
  1. No secondary sexual characteristics by 13
  2. No thelarche has not occurred by 14
  3. No menarche by 15-16
  4. When menses has not begun 5 years after onset of thelarche
54
Q

What are the 3 causes of delayed puberty?

A
  1. Hypergonadotropic hypogonadism = FSH >30 mIU
    1. Primary amenorrhea WO secdonary sex characteristics
  2. Hypogonadotropic hypogonadism = FSH/LH <10 mIU
    1. Primary amenorrhea WO secdonary sex characteristics
  3. Anatomic causes (mullerian agenesis; imperforate hymen; transverse vaginal septum)
55
Q

Hypergonadotropic hypogonadism (FSH >30 mIU/mL) is a cause of delayed puberty associated with what disease in females?

A

Gonadal dysgenesis (Turner Syndrome)

56
Q

What is primary amenorrhea?

A
  1. No menstruation by 13 W/O secodnary sex characteristics
  2. No menstruation by 15 W secondary sex charcteristics.
57
Q

What is secondary amenorrhea?

A

No period 6 months after last.

58
Q

After hx and PE of patient with primary amenorrhea, what do you check for next and how does this dictate the rest of your work-up?

A
  1. Are secondary sex characterstics present
    • Absent => measure FSH/LH
    • Present => do a US to see if uterus is present
59
Q

When would we expect to see hypogonadotropic hypogonadism?

  • Primary amenorrhea?
  • Secondary sex characterstics?
  • Follow up?
A
  1. Pt presents with primary amenorrhea WITHOUT secondary sex characteristics
  2. Measure FSH/LH: <10 mIU
60
Q

List 6 underlying etiologies responsible for hypogonadotropic hypogonadism (FSH + LH <10 mIU/mL).

A
  1. - Constitutional (physiologic) delay = MCC
    • Kallmann syndrome
    • Anorexia/extreme exercise
    • Pituitary tumors/disorders
    • Hyperprolactinemia
    • Drug use
61
Q

What is Kallman syndrome?

A
  • Mutations of the [KAL gene on the XChr] that prevents GnRH neurons from migrating into hypothalamus, causing hypogonadtropic/hypogonadism, anosmia and hyposmia (absent or decreased smell).
62
Q

When would we expect to see hypergonadotropic hypogonadism?

  • Primary amenorrhea?
  • Secondary sex characterstics?
  • Follow up?
A
  • Pt presents with primary amenorrhea WITHOUT secondary sex characteristics
  • Measure FSH/LH: > 30 mIU
63
Q

If a pt has primary amenorrhea WO secondary sexual characteristics, FSH/LH are > 30mIU, what is the dx and what is done NEXT?

A
  • Hypergonadotropic/hypogonadism
  • Karyotype analysis is performed next.
    • 46 XX => Premature ovarian failure
    • 45 XO => Tuners syndrome/gonadal dysgenesis
64
Q

If karyotype of pt with hypergonadotropic hypogonadism comes back with a Y chromosome, what is the next best step?

A

Gonadectomy to prevent malignant neoplastic transformation

65
Q

What is the most common form of female gonadal dysgenesis and what does it cause?

A

Turner Syndrome (45 XO) = hypergonadotropic/hypogonadism = many will show NO signs of secondary sex characterstics.

66
Q

Signs of Turners Syndrome? (6)

A
  1. Web neck (pteryguim colli)
  2. Broad-flat chest with widely spaced nipples
  3. Short
  4. Rudimentary streaked ovaries
  5. Absent or incomplete development of puberty
  6. Coarctation of aorta
67
Q

If a pt has [primary amenorrhea with secondary sexual characteristics], but US reveals an absent or abnormal uterus, what test is done next and what are you looking for?

A
  1. Karyotype analysis
  • 46, XY = Androgen insensitivity syndrome (AIS)
  • 46, XX = Mullerian agenesis
68
Q

What is the karyotype seen w/ Androgen Insensitivity Syndrome (AIS) and what are some characteristics seen in females with this disorder?

A
  • 46 XY => male levels of testosterone
  1. External female genitalia w/ absent to sparse pubic hair with testes in abdominal wall that secrete NL antimullerian hormone =>
  2. NO uterus and upper vagina
  3. Breast development w/ smaller than normal areola/nipples
69
Q

Tx for androgen insensitivity syndrome (46,XY)?

A
  1. Gonadectomy after puberty to avoid neoplasm
  2. Can create neovagina by surgical and non-surgical methods
  3. +HRT
70
Q

What is the most common cause of primary amenorrhea in women with normal breast development?

A

Mayer-Rokitansky-Kuster-Hauser Syndrome (Mullerian agenesis)

71
Q

What is the karyotype and characteristics of Mayer-Rokitansky-Kuster-Hauser Syndrome?

A
  1. 46 XX —> female range of testosterone
  2. NO uterus and upper vagina bc distal mullerian ducts did not fuse; renal abnormalities common
  3. NL ovaries, secondary development, and external genitalia
72
Q

Congenital anomalies of the uterus or vagina are often associated with abnormalities of _________ and should be assessed with ______.

A

Renal abnormalities

Intravenous pyelogram = to assess urinary system

73
Q

Patient presents with

  • Primary amenorrhea + secondary sex characterstics
  • US = NL/present uterus
  • What do we assess for next and DDx?
A
  • Is an outflow obstruction present?
    • Yes => imperforate hyman or transverse vaginal septum
    • No => Evaluate for secondary amenorrhea.
74
Q

What should you suspect in adolescents that present complaining of monthly dysmenorrhea without vaginal bleeding; a vaginal bulge and midline cystic mass?

A

Imperforate hymen

75
Q

Although the presentation of sx’s will be similar btw imperforate hymen and transverse vaginal septum, what is one difference?

A

Transverse vaginal septum will NOT have vaginal bulge

76
Q

How do we confirm and treat imperforate hymen?

A
  • Confirm: US and hematocolpos
  • Treat: Hymenectomy
77
Q

How do we dx and treat transverse vaginal septum?

A
  • DX = MRI
  • Treat: Surgery
78
Q

List 4 labs that should be ordered for patient with secondary amenorrhea?

A
  1. Urine hCG (ALWAYS!!!)
  2. TSH
  3. FSH
  4. Prolactin
79
Q

When a patient presents with [secondary amenorhea = w/o a period for 6 months of last], what are the next steps we do?

A
  1. Pregnancy test. If negative,
  2. Check TSH/Prolactin
    1. ​NL prolactin, ABNL TSH => hypothyroidism
    2. NL TSH, ABNL prolactin =>
      1. Prolactin >100 ng/mL => perform MRI to eval prolactinemia
      2. Prolactin < 100 ng/mL => look for other causes
    3. Both NL
      1. Progesterone challenge test
        1. Positive = bleeding occurs => normogondatropric hypogonadism (PCOS is MC)
        2. Negative = no bleeding occurs => means inadequate estrogen or outflow tract abnormality
          1. Estrogen progesterone challenge test => takes 21 tests
            1. Negative = outflow tract obstruction
            2. Positive = ABNL HPO axis
              1. Check FSH/LH
                1. High => hypergonadotropic hypogonadism => ABNL ovary
                2. NL/low => hypogonatropic hypodonadism => pituiary or hypothalamic abnormality
                  1. MRI
                    1. No tumor => hypothalamic cause
80
Q

What do you do if prolactin/TSH are both NL?

A

Both NL

  • Progesterone challenge test
    • Positive = bleeding occurs => normogondatropric hypogonadism (PCOS is MC)
    • Negative = no bleeding occurs => means inadequate estrogen or outflow tract abnormality
      • Estrogen progesterone challenge test=> takes 21 tests
        • Negative = outflow tract obstruction
        • Positive = ABNL HPO axis Check FSH/LH
          • High => hypergonadotropic hypogonadism => ABNL ovary
          • NL/low => hypogonatropic hypodonadism => pituiary or hypothalamic abnormality
            • Conduct MRI
              • No tumor => hypothalamic cause
81
Q

Which test is done clinically in pt with seconary amenorrhea and normal TSH/prolactin; what is a positive and negative test?

A
  • Progesterone challenge test (PCT) —> takes 7-10 days
  • Positive PCT = bleeding –> normogonadotropic hypogonadism; most commonly due to PCOS
  • Negative PCT = no withdrawl bleeding; indicates inadequate estrogenization or an outflow tract abnormality
82
Q

If an estrogen/progesterone challenge test is (+), but there is elevated FSH and LH, this indicates the abnormality is where?

A

Ovarian

83
Q

What drug is most often used for the progestin challenge test (PCT)?

Dose and duration

A
  • Medroxyprogesterone acetate (Provera)
    • 10 mg po qd
    • 7-10 days
84
Q

What drugs are used for estrogen/progestin challenge test?

A
  1. Conjugated equine estrogen (premarin)
  2. Estradiol (estrace)

Followed by progestin

Takes 21 days

85
Q

Outflow obstruction seen in secondary amenorrhea can be due to what?

A
  1. Asherman syndrome
  2. Cervical stenosis
86
Q

What type of menorrhea is mild hypothyroidism associated with>

A
  1. Hypermenorrhea
  2. Oligomenorrhea
  3. Treatment reverses
87
Q

What is the most common sx of hyperprolactinemia?

A

Galactorrhea = spontaneous flow of milk from breast

88
Q

What should be done if we have REALLY HIGH hyperprolactinemia (>100 ng/mL)?

Common causes?

A
  • MRI of the head
    1. Pituitary adenoma
    2. Empty sella syndrome
89
Q

What type of pituitary adenomas can we find on MRI?

A
  1. Microadenoma (<10 mm) on MRI
    1. Slow growing and rarely malignany
    2. Treat: manage symptoms and DA agonist: Bromocriptine/Parlodel
  2. Macroadenoma (>10 mm)
    1. Treat: DA agonists
90
Q

+ progestin challenge test means that our diagnosis is _____

A
  • Normogondotropic hypogonadism
      1. Nonclassical congenital adrenal hyperplasia = no genital abnormalities!!!
      1. Cushings
      1. Adrenal secreting tumor (DHEA-S > 7000 ng/mL)
    • 4. PCOS = MOST COMMON
91
Q

What is the leading cause of female anovulatory infertility?

A

Polycystic ovarian syndrome (PCOS)

92
Q

60-70% of patients with PCOS will have what symptoms?

A

Insulin sensitivity => insulin hypersecretion

93
Q

Diagnosis of PCOS needs to meet 2 of which 3 criteria?

A
  1. Oligomenorrhea or amenorrhea
  2. Biochemical or clinical signs of hyperandrogenism: LH to FSH (2:1)
  3. U/S revealing multiple small cysts beneath cortex of the ovary
94
Q

What is the effect of elevated insulin and androgen levels in pt’s with PCOS?

A

↓ the liver prod. of sex hormone binding globulins (SHBG) —> ↑ in circulating testosterone

95
Q

Increase LH; decrease FSH in PCOS causes what?

A
    1. Decrease follicular maturation and stimulation of stroma and theca cells
      * 2. Decrease follicular maturation => chronic anovulation
      * 3. Stim. of strom and theca cells => excess of androgens
      • => excess of androgens go to adipose tissue => extraglandular aromatization that increases estrogen production => increase in LH; decrease in FSH
96
Q

Chronic anovulation in PCOS causes what?

A

=> unoppsed estrogen => increase risk of endometrial cancer

97
Q

What are some of the treatment options for PCOS?

A
  1. Weight loss!
  2. Oral contraceptives –> suppress FSH and LH –> ↓ testosterone and estrogen will ↑ SHBG
  3. Clomiphene citrate can induce ovulation
  4. Ovarian diathermy/laser tx
  5. Spironolactone and/or electrolysis
  6. Metformin = insulin-sensitizing agent
98
Q

If a progesterone challenge test (PCT) is (-) and a estrogen (PCT) test is (+), what levels should be checked next?

A

FSH and LH levels

99
Q

Estrogen PCT is positive => check FSH/LH levels. Results tell us what?

A
    1. FSH > 20 IU and LH > 40 IU => hypergonadotropic hypogonadism
      * 1. Menopause if over 40 (postmenopausal ovarian failure)
      * 2. Premature ovarian failure if before 40
    1. FSH and LH are <5
      * => perform MRI
      • Tumor => pituiary tumor
      • NL => hypogonadotropic hypogonadism
100
Q

In evaluating a female pt with hyperandrogenism what should be suspected if the DHEA-S levels are >7000 ng/mL?

A

Adrenal androgen producing tumor

101
Q

In evaluating a female pt with hyperandrogenism what should be suspected if the total testosterone is >200 ng/dL?

A

Ovarian androgen producing tumor

102
Q

Difference between hirsutism and virilization?

A
  1. Hirsutism => excess terminal hair in a male pattern bc hair follicles are exposed to excess androgens.
    1. Not always pathological
  2. Virulization => masculinzation of a F associated with marked increase circulating testosterone due to excess M hormones
103
Q

Why is acanthosis nigricans a common finding in women with PCOS?

A

Due to the ↑ insulin resistance and hyperinsulinemia

104
Q

Look at levels of ____ to exclude CAH.

A

17-hydroxyprogesterone level

105
Q

Define polymenorrhea and oligomenorrhea?

A
  • Polymenorrhea = cycles <21 days causing abnormally frequent menses
  • Oligomenorrhea = menstrual cycles occuring >35 days but less than 6 months
106
Q

Define menorrhagia, metrorrhagia, and menometrorrhagia.

A
  1. Menorrhagia = heavy and/or prolonged bleeding (>80 mL and >7 days) occurring at normal intervals
  2. Metrorrhagia = irregular episodes of bleeding
  3. Menometrorrhagia = heavy and irregular bleeding
107
Q

What is intermenstrual bleeding?

A

Scant bleeding at ovulation for 1 or 2 days.

108
Q

What is DUB (dysfunctional uterine bleeding)?

A
  • Abnormal uterine bleeding usually due to aberrations in HPO axis, causing anovualation. Cannot be due to:
    • Meds, coagulopathies, systemic diseases, trauma, organic
109
Q

When does most DUB occur?

A
  1. Around years of menarche (11-14 YO)
  2. Perimenopause (45- 50YO)
110
Q

What is the PALM-COEIN classification system for abnormal bleeding in reproductive aged women?

A
  • Polyps (AUB-P) - Coagulopathy (AUB- C)
  • Adenomyosis (AUB-A) - Ovulatory dysfunction (AUB-O)
  • Leiomyoma (AUB-L) - Endometriosis (AUB-E)
  • Malignancy and hyperplasia (AUB-M) - Iatrogenic (AUB-I)
  • Not yet classified (AUB-N)
111
Q
  1. AUB- C is associated with _______.
  2. AUB- O is associated with _______
A
  1. Heavy flow
  2. Unpredictable menses with variable flow (PCOS)
112
Q

What are availble tissue sampling methods for abnormal uterine bleeding?

A
  1. Office endometrial biopsy***
  2. Hysteroscopy directed endometrial sampling
113
Q

What is the treatment for abnormal MASSIVE uterine bleeding?

A
  1. Hospitalization and transfusions if hemodynamically unstable
  2. 25 mg IV conjugated estrogens then hormonal tx (Mirena)
114
Q

What is the treatment for abnormal uterine bleeding when moderate amount of blood?

A

Combination OCP’s, Mirena

115
Q
A

Endo/Repro II Test 1 (23 decks)

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