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Paeds and Adolescent Gynae > Amenorrhoea, HMB and dysmenorrhoea in adolescence > Flashcards

Amenorrhoea, HMB and dysmenorrhoea in adolescence Flashcards

1
Q

What is primary amenorrhoea

A

Absence of menstruation by age 15

OR abscence of menstruation by age 13 in the abscence of secondary sexual characteristics

OR > 3 years after start of thelarche

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2
Q

What is the incidence of primary and secondary amenorrhoea?

A

primary 0.1-0.3%

secondary 3-4%

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3
Q

What is the incidence of imperforate hymen?

A

1:4000

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4
Q

How does imperforate hymen present?

And transverse vaginal septum?

A

Primary amenorrhoea and cyclical pelvic pain

Urinary retention secondary to urethral compression from the distended vagina (haematocolpos)

Examination shows a bulge at the introitus with blood pooled behind a thin membrane

In contrast transverse vaginal septum is thicker and often higher within the vagina and usually not visible on inspection of the external vulva.

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5
Q

What % of cycles are anovulatory in the first year after menarche?

A

85%

Cycles can remains highly irregular for the first 2 years.

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6
Q

What % of adolescent women have ovulatory cycles by:

  • Two years post menarche
  • Two to four years post menarche
  • Four to five years post menarche
A
  • Two years post menarche 18-45%
  • Two to four years post menarche 45-70%
  • Four to five years post menarche 80%
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7
Q

Describe your approach to prescribing NSAID for primary dysmenorrhoea including mechanism of action

A

NSAID is first-line therapy if contraception is not desired.

Mechanism of action: COX-2 inhibitor; COX-2 produces PGs causing inflammation and pain.

How to take: start at onset of menses and continue for duration of pain; if severe commence a few days before expected menses.

Side-effects: GI upset and bleeding; advise to take with food.

If one class if NSAID is not effective, try another class.
Classes:
- Propionic: ibuprofen, naproxen
- Fenamate: mefenamic acid

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8
Q

What are the top three causes of primary amenorrhoea?

A

Gonadal dysgenesis (46%) - 45 XO, 46XX (POI), 46XY GD

Mullerian agenesis (15%) - MKRH

Physiological delay of puberty (14%) - Constitutional, chronic systemic illness, acute illness

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9
Q

You are investigating a woman for hyperandrogenism: What investigations would you perform?

How might the androgen panel results suggest an origin of the hyperandrogenism?

A
  • Testosterone, SHBG, FAI, LH:FSH ratio - PCOS
  • DHEA, DHEA sulfate - High levels of DHEA and DHEA sulfate suggest andrenal origin.
  • 17-OH progesterone - CAH
  • Dexamethasone supression test - Cushing’s
  • CT/MRI adrenal: look for tumours if very high adrenal androgens.
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10
Q

Key points in clinical history and examination for primary amenorrhea

A

History should focus on:

  • chronology of pubertal changes,
  • eating and exercise patterns,
  • weight change,
  • chronic illness,
  • medication use,
  • sexual activity
  • symptoms of galactorrhea, thyroid dysfunction and androgen excess
  • Family history should include age at menarche and menopause, genetic disorders and developmental delay.

Physical examination includes:

  • assessment of habitus,
  • breast development,
  • hirsutism,
  • Turner stigmata,
  • thyroid palpation
  • examination of genitalia.
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11
Q

Initial investigations for primary amenorrhea.

A
  • Serum BHCG
  • TFT, prolactin, FSH, estradiol,
  • Pelvic USS
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12
Q

After inital investigations the prolactin is elevated. What are your next steps of management?

A
  • Check for hypothyroidism as a cause of falsely elevated prolactin
  • Neurological exam for signs of pituitary adenoma (bitemporal hemianopia)
  • Arrange MRI brain
  • Refer to endocrinologist
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13
Q

A pelvic USS shows an absent or rudimentary uterus.

What are your next steps of investigation?

What are the possible diagnoses?

A
  • Arrange karyotype and serum testosterone level
  • Differentials:
    • 46XX and female range testosterone = MRKH
    • 46XY and male range testosterone = AIS
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14
Q

Primary amenorrhea.

After initial investigations, the TSH, prolactin, BHCG and pelvic USS are normal. The FSH is elevated and the estradol is low.

What is the cause?

What are the next steps of investigation?

A

Primary ovarian insufficiency

Investigations:

  • Karyotype for chromosomal causes
    • Turners 45XO mosaicism
    • Pure gonadal dysgenesis 46XX
    • Swyers 46XY

If normal karyotype:

  • FMR1 premutation (fragile X premutation)
  • Hearing test (perault syndrome)
  • TPO-Abs (autoimmune oopheritis)
  • 21-OH Abs (commonest autoimmune cause of adrenal enzymatic dysfunction)
  • Check history for mumps, endocrine sx, FHx
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15
Q

What are the causes of primary ovarian insufficiency?

A
  • Chromosomal
    • Turners syndrome (45XO or mosaicisms)
    • Swyers syndrome (46 XY)
    • Pure gonadal dysgenesis (46XX)
    • X chromosomal structural anomalies
  • Single gene mutations
    • Fragile X syndrome
    • Galactosemia
    • Perrault syndrome
    • Blepharophimosis-ptosis-epicanthosis syndrome
  • Enzyme deficiencies in oestrogen production pathway
    • Aromatase
    • 17a hydroxylase, 17,20 lyase
  • Autoimmune
    • Autoimmune thyroiditis (hashimotos)
    • Lymphocytic oopheritis
  • Injury
    • chemotherapy/ radiotherapy
    • Mumps oopheritis
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16
Q

Primary amenorrhea.

After initial investigations, the TSH, prolactin, BHCG and pelvic USS are normal. The FSH and the estradol is low.

What is the cause?

What are the next steps of investigation?

A

Hypogonadotrophic-hypogonadism

  • Screen FHx for constitutional delay
  • Screen for eating disorders/low BMI/extreme exercise
  • Brain MRI
  • Smell assessment +/- molecular genetic screening for kalmans syndrome
17
Q

What are the causes of hypogonadotrophic hypogonadism?

A
  • Idiopathic (commonest)
  • Constitutional delay
  • Low BMI / energy deplete (via leptin and kisspeptin pathway)
  • Kallmans syndrome (KAL1 genetic mutation and others)
  • Brain tumours
  • Archnoid cysts
  • Previous injury
    • Trauma or bleed
    • Chemotherappy / radiotherapy
    • Secondary arachnoid cyst formation
18
Q

Primary amenorrhea.

After initial investigations, the TSH, prolactin, BHCG and pelvic USS shows a uterus. The FSH is normal and the estradol is normal/low.

What is the cause?

What are the next steps of investigation?

A

Menstrual outflow obstruction

OR

Hyperandrogenic states (>70% are PCOS)

Investigations:

  • FAI, testosterone, SHBG (PCOS)
  • 17-OH progesterone (CAH)
  • DHEA (adrenal androgens)
  • 24 hours urine cortisol, or 1mg dexamethasone supression test (cushings)
  • Consider adrenal imaging for tumours, particulalry in markedly elevated androgens
19
Q

What proprtion of adolescents with chronic pelvic pain will have endometriosis.

A

Over 30%

If chronic pain does not respond to ussual management for dysmennorhea, consider diagnostic laparoscopy as per manaegment in adults

20
Q

What are the inital management options for HMB in adolescence?

A

Non-hormonal

  • NSAIDS, including mefanamic acid
  • Tranexamic acid

Hormonal

  • COCP (first-line)
  • Cyclical oral progesterone for at least 21 days during luteal phase
  • Depo-provera (second-line due to concerns re. reduction in BMD)
  • Mirena IUS (but often requires GA for insertion)
  • Progesterone implant (but less effective)
21
Q

What is the definition of HMB?

A

Blood loss >80ml/day (normal is 30-40ml/day).

Clinical definition (more useful) is reported heavy vaginal bleeding AND evidence of anaemia OR patient reported effects on physcial, pyschological, emotional or material well being. (RCOG)

22
Q

What is the incidence of bleeding abnormalities in adolescents presenting with HMB?

A

20%

23
Q

What investigations should be considered for HMB in adolescents? When should it be considered?

A
  • FBC
  • clotting screen
  • VWF
  • Factor VIII
  • pelvic USS

Treatment can ususally be commenced prior to investigations, unless:

  • history of bleeding is significant
  • signs of anaemia
  • FHx bleeding conditions
  • Bleeding requiring hospital admission
  • Bleeding refracrory to usual treatment
24
Q

Investigations for coagulation defect?

A

FBC - may have low platelets (in VWD type 2a due to abnormal affinity to and sequestration of VWF)
Clotting - low APTT in VWD
VWF antigen
Factor VIII
Ristocetin co-factor (measure platelet activation)

25
Q

Treatment for VWD and HMB?

A

Medical:

  • COCP (as effective as DDAVP, increases fibrinogen, prothrombin, factor VII, factor VIII and/or vWF)
  • TXA
  • DDAVPP (Desmopressin) - causes release of VWF from endothelial cells and platelets increasing circulating levels
  • Factor VIII and/or VWF replacement
  • Mirena
26
Q

Epidemiology and inheritance of VWD

A

Prevalence = 1% (though only 0.1% symptomatic)

Most cases autosomal dominant, though rarer subtypes can be autosomal recessive

27
Q

What is the management for primary ovarian insufficiency?

A
  • Puberty induction can start from age 10
  • Always start with low dose transdermal estradiol patches, gradually increasing doses for 2-3 years (can be shortened to 6-12 months if late/adolescent presentation)
  • Then introduce cyclical progesterone e.g. provera or micronised progesterone for 14 days during luteal phase OR use COCP
  • Will require hormone replacement until the age of normal menopause for CVD and bone protection
  • Will need donors eggs and IVF for future fertility
  • Gonadectomy should be advised for all women with a Y chromosome due to increased risk of gonadoblastoma and malignancy in streak gonads.
28
Q

What are the management conisderations for hypogonadotrophic-hypoginadism?

A
  • Induction of puberty with oestogen for 2-3 years, then introduction of cyclical progesterone
  • long-term oestrogen-progestin replacement required
  • Ovulation induction with exogenous gonadotrophins is a first-line reproductive option.

Tumours:

  • surgical resection

Hyperprolactinemia:

  • Dopamine agonists (cabergoline) are the first-line management - act on D2 recpetor of anterior pituitary to reduce prolactin secretion

Paeds and Adolescent Gynae (8 decks)

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