Polycystic Ovarian Syndrome Flashcards

1
Q

What are the primary causes of Amenorrhoea? (absence of menarche by age 15)

A
  • Genitourinary abnormalities (for example, congenital absence of uterus, cervix or vagina eg Rokitansky syndrome or androgen insensitivity syndrome)
  • Chromosomal abnormalities, eg turner’s syndrome
  • Secondary hypogonadism (pituitary cause) eg, Kallmann syndrome, pituitary disease or hypothalamic amenorrhoea.
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2
Q

What are some secondary causes of Amenorrhoea? Important card (absence of more than 3 cycles)

A
  • Uterine eg, Ashermans syndrome (adhesions)
  • Ovarian eg, PCOS or premature ovarian failure,
  • Pituitary eg Prolactinoma or pituitary tumour,
  • Hypothalamic eg, weight loss, stress, or drugs
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3
Q

What are some miscellaneous causes of amenorrhea

A
  • Pregnancy or lactation,
  • Iatrogenic,
  • Thyroid dysfunction,
  • Hyperandrogenism eg, Cushings, CAH or adrenal/ovarian tumour.
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4
Q

What is the typical presentation of Polycystic ovarian disease?

A
  • Anovulation (amenorrhoea, oligomenorrhoea or irregular cysts).
  • Hyperandrogenism (hirsuitism, acne and alopecia)
  • Obesity
  • Acanthosis Nigricans
  • Raised testosterone and LH
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5
Q

What factors are involved in the pathophysiology of PCOS?

A
  • Abnormal gonadotrophins,
  • Androgen excess
  • Insulin resistance
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6
Q

Explain the gonadotrophin levels seen in PCOS

A
  • Increased LH concentration and/or increased LH receptors on ovaries. LH supports theca cells which increases ovarian androgen production.
  • Decreased FSH levels at a low constant level (instead of normal fluctuations) which results in continuous stimulation of follicle’s without ovulation. Decreased conversion of androgens to oestrogens in granulosa cells.
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7
Q

What androgens are seen to be increased in PCOS and where are these produced?

A
  • DHEA (both ovary and adrenal glands but predominantly produced by adrenal gland),
  • Androstenediol,
  • Androstenedione (both ovary and adrenal gland - predominantly ovarian),
  • Testosterone (both ovary and adrenal but predominantly ovary)
  • Dihydrotestosterone (produced in periphery by conversion of testosterone)
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8
Q

What are the precursors for testosterone?

A
  • Androstenediol(produced from DHEA)
  • Androstenedione (produced from DHEA)
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9
Q

What happens to androgen levels in PCOS?

A
  • There is increased androgen production from theca cells due to high LH,
  • Disordered enzyme action
  • Decreased sex hormone binding globulin (produced by liver), increasing amount of free testosterone - Only free testosterone is biologically active
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10
Q

What are the features of insulin secretion/sensitivity in PCOS?

A
  • Patients usually have excess insulin which causes insulin resistance and stimulates the theca cells to produce more testosterone and reduces liver production of SHBG. So there is more free testosterone
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11
Q

What are the investigations for PCOS?

A
  • Hormone profile for PCOS = High testosterone, high andrestenediol, high DHEA, high LH, low SHBG, low FSH.
  • Assess for type 2 diabetes
  • Exclude other pathologies
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12
Q

What is the treatment for PCOS

A
  • Combined oral contraceptive pill (Dianette) to regulate periods.
  • Corticosteroids in severe hyperandrogenism to suppress adrenal androgen production.
  • Spironolactone or cyproterone acetate which are androgen receptor antagonists,
  • Finasteride (alpha reductase inhibitor) reduced peripheral conversion of testosterone.
  • Weight loss!
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13
Q

What is the Rotterdam criteria for PCOS?

A

Diagnosis of PCOS can be made if has two of following:
1. Infrequent or no ovulation,
2. Clinical/biochemical signs of hyperandrogenism
3. Polycystic ovaries on US (>12 follicles in one or both ovaries)

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14
Q

What are the investigations for PCOS?

A
  1. Serum 17-hydroxyprogesterone (to exclude 21 hydroxylase deficient adrenal hyperplasia)
  2. Serum prolactin (exclude Hyperprolacinaemia which can present with irregular periods).
  3. TSH (exclude thyroid pathology which can cause abscent/irregular/heavy periods)
  4. OGTT.
  5. Fasting lipid profile
    Others may include: testosterone, DHEA, pelvic ultrasound,
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