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203: Theme 2 > Disorders of Ovalution > Flashcards

Disorders of Ovalution Flashcards

1
Q

Review the phases of ovulation

A
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2
Q

What is the role of Kisspeptin in the regulation of Ovulation?

A
  • it’s a GnRH secretagogue found at the apex of the reproductive axis in the hypothalamus
  • KISS1 neurons are highly responsive on oestrogen
  • it is implicated in +ve and -ve central feedback of sex steroids on GnRH production
  • there are also metabolic influences via
    • leptin
    • has permissive effects on puberty & reproduction
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3
Q

How would you diagnose/ identify ovulation?

A
  • via Biochemistry:
    • 7 days before start of next menstrual period a progesterone blood test is taken
    • LH detection kits: urine sample (over the counter)
  • via Transvaginal pelvic ultrasound:
    • done form day 10 of ovulation cycle, to look at the developing follicle size of the corpus luteum
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4
Q

Define the following terms

  • Amenorrhoea
  • Primary Amenorrhoea
  • Secondary Amenorrhoea
  • Oligomenorrhoea
  • Polymenorrhoea
A
  • Amenorrhoea - lack of a period for more than 6 months
    • Primary Amenorrhoea - never had a period (never went through menarche)
    • Secondary Amenorrhoea -has menstruated before
  • Oligomenorrhoea - irregular periods
    • usually occurring more than 6 weeks apart
  • Polymenorrhoea - periods occurring less than 3 weeks apart
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5
Q

What are the Pituitary causes of ovulation problems?

A
  • Pituitary (lack of FSH and LH)
    • pituitary tumours (prolactinoma/other tumours)
    • post pituitary surgery /radiotherapy
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6
Q

What are the Hypothalamic causes of ovulation problems?

A
  • Hypothalamus (lack of GnRH)
    • GnRH deficiency (Kallmann’s syndrome)
      • may be associated with anosmia (lack of sense of smell)
    • ‘Functional’ hypothalamic amenorrhoea
      • weight loss/stress-related/excessive exercise
      • anorexia nervosa/bulimia
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7
Q

What are Ovarian causes of ovulation problems?

A
  • Premature ovarian insufficiency
    • Chromosomal abnormalities eg Turner syndrome
    • Autoimmune (endocrine conditions, familial link)
    • Iatrogenic
      • Surgery/chemotherapy/radiotherapy
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8
Q

What is Hyperandrogenism?

A
  • excessively high male sex hormones e.g
    • PCOS: polycystic ovarian syndrome
    • Cogenital adrenal hyperplasia
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9
Q

What is Hirsutism?

A
  • Androgen-dependent excess body hair in a male distribution
  • there is androgen-independent hair growth: Hypertrichosis
  • their a familial and racial links to the pattern of hair growth
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10
Q

What is a differential diagnosis for hirsutism?

A
  • 95% - PCOS or ‘idiopathic hirsutism’
    • occurs in 5-10% of women
  • 1% - Non-classical congenital adrenal hyperplasia (CAH)
  • <1% - Cushing’s syndrome
  • <1% - Adrenal / ovarian tumour
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11
Q

When would presentation of Hirsutism symptoms be problematic/ worrying?

A
  • Sudden onset of severe symptoms compared to a life long PCOS diagnosis
  • if it was associated with Virilisation (more sever impact of male hormones)
    • Frontal balding
    • Deepening of voice
    • Male-type muscle mass
    • Clitoromegaly
  • Possible Cushing’s syndrome requires more investigation
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12
Q

What are the clinical features of PCOS?

A
  • Hyperandrogenism
    • causing hirsutism and acne
  • Chronic oligomenorrhoea/amenorrhoea
    • nine or fewer periods a year
    • subfertility
  • Obesity (25% of women with PCOS are “lean”), obesity can make it worse
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13
Q

What is this an image of and what is it showing?

A
  • Polycystic ovaries- via a transvaginal USS
  • the dark spaces are multiple premature follicles that have sprung up instead of the usual one follicle becoming dominant before ovulation
  • not all women with PCOS with have USS appearance
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14
Q

What hormonal abnormalities are seen in PCOS?

A
  • Raised baseline LH and normal FSH levels. Ratio LH:FSH 3:1
  • Raised androgens and free testosterone (due to less SHBG)
  • Reduced Sex Hormone Binding Globin (SHBG)
    • binds testosterone and oestradiol
    • produced in the liver
    • increased by oestrogen and decreased by testosterone
  • Oestrogen usually normal
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15
Q

What potential consequences does insulin resistance/obesity present in women with PCOS?

  • Reproductive
  • Metabolic
A
  • Endocrine manifestations
    • increased insulin –> decreased liver production of SHBG
    • increased ovary and adrenal activity
      • increased androgen activity
        • Infertility/ menstrual disturbance, hirsutism
        • increased risk of Gestational Diabetes
  • Metabolic manifestations
    • Glucose intolerance
    • Dyslipidemia
    • vascular dysfunction
      • Vascular disease
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16
Q

What is the link between PCOS and Endometrial Cancer?

A
  • irregular periods coupled with high oestrogen levels can lead to endometrial hyperplasia –> increased risk of cancer
  • endometrial cancer is associated with type 2 diabetes and obesity
17
Q

What lifestyle modifications can be made to improve PCOS symptoms?

A
  • Diet & exercise
    • high risk of eating disorders so approach with sensitivity
  • Stop smoking (increases androgen levels in women)
  • RESULTS:
    • decreased insulin resistance
    • ­ increased [SHBG]
    • decreased [free testo]
    • Improved fertility/pregnancy outcomes
    • Improve metabolic syndrome risk factors
18
Q

What’s the effect of Combined Oral Contraceptives on PCOS?

A
  • increases SHBG and thus decreases free testosterone
  • decreases FSH & LH and therefore ovarian stimulation
  • regulates cycle & decreases endometrial hyperplasia
  • BUT may cause weight gain, venous thrombosis, adverse effects on metabolic risk factors
19
Q

What is the role of Anti-androgens in PCOS?

A
  • can be used with COCP / other forms of secure contraception (have a teratogenic effect)
  • Cyproterone Acetate (oral tablet)
    • inhibits binding of testosterone & 5 alpha dihydrotestosterone to androgen receptors
  • Spironolactone (oral tablet)
    • anti mineralocorticoid and anti-androgen properties
20
Q

Explain targeting insulin resistance in PCOS

A

Metformin

  • decreased insulin resistance decreased insulin levels –> decreased ovarian androgen production
  • may help with weight loss/ diabetes prevention
  • may increase ovulation frequency (with clomifene) (safe in pregnancy)
  • less helpful for hirsutism & oligomenorrhoea but may be an option in obese women
21
Q

What treatment can be given to women with Hirsutism?

A
  • mechanical hair removal is usually required
    • Photepialtion/ electrolysis
  • Eflornithine cream (non-NHS, cost, lack of efficacy)
    • inhibits ornithine decarboxylase enzyme in hair follicles
22
Q

What is the treatment of ovulation for women with PCOS?

A

Clomifene

23
Q

How would Primary Ovarian Insufficiency present?

A
  • Primary or secondary amenorrhoea
    • Secondary amenorrhoea may be associated with hot flushes & sweats
  • Other terms used:
    • Premature ovarian failure
    • Premature menopause
24
Q

What is the aetiology of Primary Ovarian Insufficiency?

A
  • Autoimmunity
    • May be associated with other autoimmune endocrine conditions
  • X chromosomal abnormalities
    • Turner syndrome
    • Fragile X associated
  • Genetic predisposition
    • Premature menopause
  • Iatrogenic
    • Surgery, radiotherapy or chemotherapy
25
Q

What investigations can be done in Premature Ovarian Failure?

A
  • history / examination
  • ­increased LH and FSH, repeat at least once not at 14 days intervals
  • ? Karyotype
  • Consider pelvic USS
  • Consider screening for other autoimmune endocrine diseases
    • Thyroid function tests, glucose, cortisol
26
Q

What is the management for Premature Ovarian Failure

A
  • Psychological support: daisy network
  • Hormone Replacement Therapy (HRT)
    • Continue till ± 52
    • reduces hot flushes and other symptoms, can maintain bone health
  • Monitor bone density
    • DEXA scan
  • Fertility tx
    • IVF with donor egg
27
Q

What is Turner Syndrome?

  • genetic presentation
  • general presentation/ diagnosis?
A
  • Complete / partial X monosomy in some / all cells
    • 50% of cases will be XO
    • Rest: partial absence of X or mosaicism
  • occurs in 1:2000 – 1:2500 live-born girls
  • Presentation
    • May be diagnosed in the neonate/ various stages
    • May present with short stature in childhood
    • May present with primary / secondary amenorrhoea
28
Q

What are associated problems with Turner Syndrome?

A
  • Short stature
    • Consider GH treatment (high dose in childhood, benefits in adulthood)
  • CV system
    • Coarctation of aorta
    • Bicuspid aortic valve
    • Aortic dissection
    • Hypertension (adults)
  • Renal
    • Congenital abnormalities
    • single horseshoe kidney
  • Metabolic syndrome
  • Hypothyroidism
  • Ears/hearing problems
    • usually ​high-frequency hearing loss
  • Osteoporosis (lack HRT)
29
Q

What is Congenital adrenal hyperplasia (CAH)?

A
  • disorders of cortisol biosynthesis
    • high Carrier frequency of 1 : 60
    • Most patients are compound heterozygotes
      • Different mutations on two alleles
  • 95% CAH cases caused by 21-hydroxylase deficiency
    • Cortisol deficiency
    • May have aldosterone deficiency
    • Androgen excess
    • Depends on degree of enzyme deficiency
30
Q

Give an overview of how CAH presents in

  • childhood
  • adulthood
A
  • Childhood
    • classic/severe
    • salt-losing (in 2/3rd of patients)
    • non-salt losing (1/3rd of patients)
    • simple virilisng occurs
  • Adulthood
    • non-classic/ mild
    • late-onset
31
Q

How does CAH (Congenital adrenal hyperplasia) present in childhood?

A
  • Salt wasting present early in life
    • Hypovolaemia, shock
  • Virilisation
    • Ambiguous genitalia in girls
    • Early virilisation in boys (unable to determine sex)
  • Precocious puberty
  • Abnormal growth
    • Accelerated early
    • Premature fusion
32
Q

How does CAH (Congenital adrenal hyperplasia) present in adulthood?

A
  • Hirsutism
  • Oligo / amenorrhoea
  • Acne
  • Subfertility
  • Similar to ‘PCOS’ presentation
33
Q

What is the treatment for CAH (Congenital Adrenal Hyperplasia) treatment?

A
  • Glucorticoid & mineralocorticoid replacement
    • Hydrocortisone & fludrocortisone
    • Additional salt in infancy
    • Glucocorticoids suppress CRH / ACTH (which itself drives the system to produce too many androgens
  • Supraphysiological glucocorticoid doses may be needed to suppress adrenal androgen production
    • Monitor [17-OH-P] / androstenedione
    • Monitor growth in childhood
      • Excess glucocorticoid treatment may inhibit growth
  • Surgical management for ambiguous genitalia (done later in life in orderfor female to have more involvement in tx)
  • Non-classical CAH in adult women (mild)
    • Can treat as for PCOS with COCP ± anti-androgen

203: Theme 2 (11 decks)

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