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203-T2 > Disorders of ovulation > Flashcards

Disorders of ovulation Flashcards

1
Q

What do KISSpeptin and KNDY neurons do?

A

They are potent stimulates of GnRH. They are stimulated by high oestrogen and they drive LH production through stimulation of GnRH.

  • KISSpeptin synapse as median eminance

KISSpeptin/GnRH and LH are all pulsatile (60-90 minutes)

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2
Q

What does GnRH do in the release of FSH?

How is negative feedback implicated?

A

GnRH stimulates FSH which acts on the primary follicle granulosa cells which start producing oestrogen and inhibin.
- FSH increases the LH receptors in the granulosa cells

These hormones inhbit FSH. However when oestrogen is critically high then positive feedback on the KISSpeptin and KNDY neurons –> stimulation of GnRH production –> more LH production (due to high frequency and amplification of the pulse from GnRH)

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3
Q

LH triggers

A
  • ovulation
  • resumption of oocyte meiosis
  • changes to the granulosa cells into luteal cells
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4
Q

How do you diagnose ovulation by taking a history?

A
  • Regular menstruation (approx 28 days)
  • Check if on the pill
  • Mid cycle pain @ ovulation
  • Vaginal discharge alters (increased mucous post ovulation)
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5
Q

How do you diagnose ovulation biochemically?

A
  • Day 21 progesterone blood tests (7 days prior to next bleed)
  • LH detection kits: urinary (can get over the counter)
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6
Q

How do you diagnose ovulation by taking a transvagincal pelvic ultrasound?

A
  • Begin from day 10 (alternate days to demonstrate the developing follicle size and corpus luteum)

Do not take basal body temp, cervical mucus, vaginal epithelium changes nor endometrial biopsies

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7
Q

How can the hypothalamus cause ovulation problems?

A

Lack of GnRh due to

  • KISSpeptin deficiency/GnRH gene deficiency (RARE)
  • Weight loss/ stress/excessive exercise (decreases pulsatility of GnRH)
  • anorexia/ bulimia
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8
Q

How can the pituitary gland cause ovulation problems?

A

Lack of FSH and LH due to

  • Pituitary tumours (prolactinoma/other)
  • Post pituitary surgery/radiotherapy
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9
Q

How can the ovary cause ovulation problems?

A

Lack of oestrogen/progesterone due to

  1. Premature ovarian insufficiency
    - developmental/genetics eg Turners syndrome
    - AI damage
    - cytotoxic and radiotherapy
    - Surgery
  2. Polycystic ovarian syndrome (COMMONEST)
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10
Q

Define the following terms:

  1. Amenorrhoea
  2. Oligomenorrhoea
  3. Polymenorrhoea
  4. Hirsuitism
A
  1. Lack of periods for more than 6 months. (primary= never went through menarche, secondary= menstruated before)
  2. Irregular periods (usually >6 weeks apart)
  3. Periods occurring <3 weeks apart
  4. Excessive body hair in a male distribution. NOT the same as ‘androgen-independent hair growth’- hypertrichosis or familial/ racial hair growth
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11
Q

Consider the clinical features of polycystic ovarian syndrome (PCOS)

State 5 features relating to metabolic syndrome and 3 not relating to metabolic syndrome

A

METABOLIC SYNDROME

  • High risk of CVD
  • Vascular dysfunction
  • Dyslipidaemia
  • Impaired glucose tolerance (leading to increased risk of gestational diabetes or T2DM)
  • Insulin resistance with high insulin (leading to high androgen production by ovarian theca cells and low SHBG production by liver)

NON METABOLIC SYNDROME

  • Hyperandrogenism –> acne, hirsutism
  • Obesity (25% patients lean)
  • Chronic oligo/amenorrhoea (<9 periods/year) –> subfertility
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12
Q

What does the PCOS diagnostic triad consist of?

A
  • Polycystic ovaries
  • Oligo/anovulation
  • Androgen excess
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13
Q

What is the pathophysiology of PCOS?

A

High GnRH causes:

  1. High LH by theca cells –>androgen excess –> hirsutism
    - Raised baseline LH, normal FSH, free testosterone
  2. Low FSH inhibiting Granulosa cells –> follicle arrest –> anovulation
    - Low SHBG
    - Low/normal oestrogen
    - Obesity causing Insulin resistance can lead to inhibition of granulosa cells
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14
Q

What is the pathology of PCOS

A
  • Greater than 10 subcapsular follicles 2-8mm in diameter arranged around a thickened ovarian stroma.
    (not all women)
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15
Q

What is SHBG

A

Sex hormone binding globulin

  • produced by the liver
  • binds oestrogen and testosterone
  • if bound to testosterone, it is NOT active
  • increased by oestrogens
  • decreased by testosterone thus releasing more free-T
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16
Q

What are the reproductive effects of PCOS?

What are the cancer effects of PCOS?

A
  • Associated with infertility (15% of infertility cases)
  • Associated with increased miscarriages
  • Increased risk of gestational diabetes
  • Endometrial cancer risk increased due to high endometrial hyperplasia
  • Lack of progesterone on the endometrium
  • Endometrial cancer associated with T2DM and obesity
17
Q

Consider treatment for PCOS

  1. Discuss life style modification
  2. Discuss COCP. Side effects?
A
  1. Diet and exercise/ smoking cessation –> decreased insulin resistance, increased [SHBG], decreased [free T], increased fertility, improves metabolic syndrome risk factors
  2. Increased SHBG (so less [Free T]); Decreases FSH and LH (ovarian stimulation); regulated cycle and decreases endometrial hyperplasia
    - weight gain, venous thrombosis, adverse effects on metabolic risk factors
18
Q

Consider treatment for PCOS

  1. Discuss anti-androgens
  2. Discuss hair removal
A
  1. Used in combination with COCP or other form of secure contraception.
    Cyproterone acetate (oral) inhibits binding of testosterone and 5-a-dihydrotesterone to androgen receptors
    Spironolactone (oral) is an anti-mineralocorticoid and anti-androgen
  2. Laser treatment or hair removal cream
19
Q

What is primary ovarian insufficiency and how does it present?

A

Premature ovarian failure/premature menopause

Amenorrhoea (primary or secondary)
- 2ndry may by associated with hot flushes/sweats

20
Q

What is the aetiology of primary ovarian insufficiency?

A
  1. AI: may be associated with other AI endocrine disorders (X chromosome abnormalities: Turners, FragileX)
  2. Genetic predispositon (to premature menopause)
  3. Iatrogenic: surgery, radiotherapy, chemotherapy
21
Q

What investigations would you do if suspected primary ovarian insufficiency?

A
  • Hx/Examination
  • Bloods: High LH/FSH
  • Karyotype?
  • Pelvic USS
  • Screening for other AI EDs
22
Q

How would you manage a patient with primary ovarian insuffiency?

A
  • Psychological support
  • HRT (until 52)
  • Monitor bone density (dexa scan)
  • Fertility (IVF with donor egg)
23
Q

Turner syndrome is an x chromosome abnormality. Describe its genetics and presentation

A
  • Complete/partial x monosome in some/all cells (50% will be XO)
  • 1/2000-2500 girls

Presentation: droopy eyelids, high and arched palette, short stature, skeletal anomaly (wide carrying angle), primary or secondary amenorrhoea

  • Diagnosis as a neonate
  • Short stature becomes apparent in childhood (GH supplement?)
24
Q

What are the complications of turners syndrome?

A
  • CVS: aortic dissection, coarctation of the aorta, bicuspid aortic valve, hypertension
  • RENAL: congenital abnormalities
  • Osteoporosis (lack HRT)
  • Ears/hearing problems
  • Hypothyroidism
  • Metabolic syndrome
25
Q

What is the differential diagnosis for hirsuitism?

When might you exhibit a high degree of concern?

A

PCOS (95%)

Non-classical congenital adrenal hyperplasia (CAH)

Cushings

Adrenal/ovarian tumour

If sudden onset of severe symptoms, virilisation (frontal balding, deepening voice, male type muscle mass, clitoromegaly) or possible cushings

26
Q

What is congenital adrenal hyperplasia (CAH) and what is its aetiology?

A

Its a disorder of cortisol biosynthesis. Aldosterone, cortisol, dihydrotestosterone and oestradiol are all synthesised from cholesterol.

AETIOLOGY

  • Carrier frequency 1:60
  • Most patients are compound heterozygotes (different mutations in 2 alleles)
  • 95% caused by 21-hydroxylate deficiency leading to cortisol deficiency, aldosterone deficiency (sometimes) and androgen excess.

**Severity depends on enzyme deficiency

27
Q

What is the pathophysiology of CAH?

How would you diagnose it?

A

Defect in cortisol biosynthesis —> High CRH/ACTH –> excess adrenal androgen production

*High CRH/ACTH due to lack of negative feedback

Diagnosis: High [17-hydroxyprogesterone], confirm with SYNACThen test

28
Q

How does childhood presentation of CAH differ to adult presentation?

A

CHILDHOOD

  • ‘classical’/’severe’
  • salt losing (in 2/3) –> hypovolaemia/shock
  • non-salt losing
  • simple virilising (ambiguous genitalia in girls, early virilising in boys)
  • precocious puberty
  • abnormal growth (early acceleration, premature fusion)
ADULTHOOD
- 'non classical'/ 'mild'
- 'late onset'
-  Hirsutism, acne, oligo/amenorrhoea
- Subfertility
(similar to PCOS)
29
Q

Consider treatment for congenital adrenal hyperplasia/

Discuss glucocorticoid and mineralocorticoid replacement

A

e.g. hydrocortisone,fludrocortisone

  • Additional salt in infancy
  • glucocorticoid suppress CRH/ACTH
  • supraphysiological glucocorticoiddoses needed to supress adrenal androgen production (by upregulating negative feedback)
  • monitor [17-OH-P]/androstenedione
  • monitor growth in childhood (excess glucocorticoid inhibits growth)
30
Q

Consider treatment for congenital adrenal hyperplasia/

What other treatment options are there other than glucocorticoid and mineralocorticoid replacement

A
  1. Surgical management for ambiguous genitalia
  2. Non-classical CAH in adult women (mild)
    - treat as for PCOS with COCP and anti-androgen

203-T2 (19 decks)

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