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Exama-vaginologists > REI > Flashcards

REI Flashcards

1
Q

Benefits of Transdermal Estrogen replacement vs oral

A
  1. Provides 17-beta-estradiol, which is structurally identical to ovarian 17-beta-estradiol.
  2. Avoids the first-pass effect (which is a/w inc production of clotting factors).
  3. Replacement by steady infusion rather than by bolus.
  4. Reduces the risk of VTE vs oral route
  5. May be associated with a reduced risk of GB (ie, cholecystitis, cholelithiasis, and cholecystectomy)

(UTD)

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2
Q

Define Delayed Puberty and precocious puberty

A 
1. 
No breast development age 13
No menses age 15
2.
Before age 8
- < 7 caucasian
- < 6 black
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3
Q

Most common cause Delayed Puberty

A

Hyper/Hypo (43%) gonadal failure

Hypo/Hypo (31%)

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4
Q

What does breast development suggest re: eugonadism vs hypogonadism

A

No breasts = hypogonadal

breasts = preduced estrogen at some point, assess current estrogen status with progestin withdrawal test

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5
Q

Pt with Hyper/Hypo: next step

A

Karyotype

- usually abn like 45x with mosaicism or 46XY (Swyer)

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6
Q

Hypo/Hypo pt: next step

A

MRI to r/o pituitary tumor
If no Tumor DDX:
- functional
- Irreversible - hypothalamic tumor, Kallmans, IHH

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7
Q

Eugonadism and amenorrhea DDX

A

Outflow obstruction
Mullerian Aplasia
AIS - no pubes, no ut/vagina s/t AMH production
Ovulatory dysfcn (PCO, Hyperprolactinemia, Thyroid dysfcn)

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8
Q 
CASE: 
17 y/o primary amenorrhea
unable to smell
FMx infertility
Tanner 5 breast, vagina present
1. Investigations? 
2. If she had no breast development would it be different?
A

1.
- Determine current Estrogen status - Tanner 5 breast
Progestin withdrawal bleed (Provera 10 x 10) = neg
- FSH, E2, TSH, PRL
- Bone age
2.
Yes - hypogonadism present if no breasts so no need to assess E2 status

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9
Q 
CASE: 
17 y/o primary amenorrhea
unable to smell
FMx infertility and anosmia
Tanner 5 breast, vagina present
FSH 2, Provera challenge failed
1. Dx
2. Next Step
3. Likely Cause
4. Tx
A
  1. Hypo/Hypo
  2. MRI
  3. Kallman’s
    • Sex steroid replacement: Estrogen until breast development adequate then add progestin (combined OCP)
    • Calcium/Vit D
    • Gonadotropins for fertility
    • Genetic counselling
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10
Q

What is the most common mutation for idiopathic Hypo/Hypo?

A

FGFR1

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11
Q 
CASE: 
16 y/o primary amenorrhea
no breasts, short
Tanner 3 pubic hair
Declines pelvic
1. Ix
2. If Hyper/Hypo next steps
3. Likely Dx
4. Management
A
  1. FSH, TSH, PRL
  2. Karyotype
  3. Turners (45X)
    • Remove the gonads!
    • risk of cardiac /renal abn
    • risk of hypothyroidism
    • NO donor IVF - cardiac risks
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12
Q 
19 y/o primary amenorrhea
cervical spine immobility and joint pain
no pelvic pain
breasts present
Tanner 5 pubic hair
No vagina
1. DDX
2. most likely and what else to look at?
A

1.

  • transverse vaginal septum or imperforate hymen (usually have pain, younger)
  • complete AIS (usually Tanner 1-2)
  • Mullerian aplasia
    2. mullerian aplasia, kidneys
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13
Q

Usual time between thelarche and menarche

A

2-2.5 yrs

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14
Q

Which of the following aspects of puberty are HPO axis independent: thelarche, adrenarche, growth spurt, menarche?

A

Adrenarche (s/t adrenal secretion androgen)

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15
Q

Tanner Staging:

A

Breast:

  1. nothing
  2. breast bud
  3. mound
  4. secondary aoreolar mound
  5. adult

Pubic Hair:

  1. nothing
  2. sparse long hairs
  3. growth sparsely spread
  4. adult hair over mons
  5. spread to thighs
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16
Q

How is precoscious puberty divided/classified?

A
  1. Central/Gonadotropin dependent
    - idiopathic (MOST COMMON)
    - CNS abnormality
    - Chronic exposure to sex steroids (McCune- Albright Syndrome, CAH, tumor) which start as peripheral and then activate puberty
  2. Peripheral/Gonadotropin independent
    - isosexual (estrogen)
    - contrasexual (androgens)
17
Q

Causes of peripheral precocious puberty

A 
Ovarian tumors
Adrenal d/o
McCune albright syndrome
Primary hypothyroidism (rare)
Exogenous estrogen (rare)
18
Q

most common tumor causing precocious puberty

A

granulosa cell tumors (60%)

19
Q

What is McCune Albright Syndrome

A

Recurrent follicular cysts
Polyostotic fibrous dysplasia
irregular cafe au lait spots

20
Q

What is the one cause of peripheral precoscious puberty that has delayed bone age (vs advanced)?

A

Primary Hypothyroidism

21
Q

What lab results suggest early puberty?

A
  • LH>FSH
  • GnRH agonist stim test pos (LH elevated)
  • E2 elevated
  • Bone age advanced > 2SD
22
Q

Tx of central precosious puberty

A

GnRH agonist suppress FSH and LH, d/c when 11-12

No longterm issues

23
Q

CASE:
5 y/o breasts Tanner 3, pubic hair Tanner 1
75%ile for height (previously 5th)
1. Ix?

A
  • bone age
  • FSH/LH ratio
  • E2
  • TSH
24
Q

CASE:
5 y/o breasts Tanner 3, pubic hair Tanner 1
75%ile for height (previously 5th)
IX: Advanced bone age, FSH>LH (prepubertal), E2 elevated, TSH nml
1. Dx
2. next step
3. most likely Dx, what does this procude?

A
  1. Peripheral precocious puberty
  2. pelvic US
  3. granulosa cell tumor, inhibin

Exama-vaginologists (7 decks)

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