RANZCOG questions Flashcards

1
Q

Ovulation induction

a. Give a brief overview on the physiology of ovulation. (4)

A

i. The pr-eovulatory follicle has produced enough oestrogen to produce a LH surge that initiates the continuation of meiosis in the oocyte, luteinisation of the granulosa and synthesis of progesterone and prostaglandins within the follicle.
a. The LH surge results from a switch from negative feedback control of LH secretion to a sudden positive feedback effect of progesterone and oestrogen.
ii. Progesterone and the progesterone influenced midcycle rise in FSH results in rupture of the follicle and frees the oocyte.

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2
Q

b. Compare anovulation due to a pituitary microadenoma and the COCP. (2)

A

b. Pituitary microadenomas secrete prolactin that causes inhibition of the pulsatile secretion of GnRH in the hypothalamus whereas the OCP causes inhibition of gonadotropin secretion by acting on the pituitary.

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3
Q

c. What is the mechanism of action of clomiphene citrate? (5)

A

c. The mechanism of action of clomiphene:
i. Clomiphene has both oestrogen agonist and antagonist properties. In the hypothalamus and pituitary it binds to oestrogen receptors and reduces negative feedback from oestrogen, altering the pattern of GnRH secretion and in turn stimulating increased pituitary gonadotropin release driving ovarian follicular development

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4
Q

d. List the common or important side effects of clomiphene. (4)

A

d. Side effects of clomiphene
i. Transient hot flushes (10%), mood swings, breast tenderness (2%), pelvic pressure or pain (5%), nausea (2%) and visual disturbance (2%)
ii. Can cause optic neuropathy
iii. Multiple pregnancy (5-8%)
iv. Ovarian hyperstimulation (rare)

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5
Q

PCOS

a. What is the approximate population incidence? (1)

A

a. The approximate incidence of PCOS is 6-8%

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6
Q

b. What are the Rotterdam Criteria for the diagnosis of PCOS? (4)

A

b. The Rotterdam criteria are two out of the three:
i. Oligo- and/or anovualtion
ii. Clinical and/or biochemical signs of hyperandrogenism
iii. Polycystic ovaries on USS (12 or more follicles is each ovary measuring 2-9mm and/or increased ovarian volume (>10ml))

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7
Q

c. List the options for a woman with PCOS and anovulation infertility? (6)

A

c. Management options for PCOS and anovulatory infertility:
i. Weight loss
ii. Ovulation induction with clomiphene (80% respond and 50% conceive)
iii. Metformin
iv. Ovulation induction with exogenous gonadotropins (72% respond and 45% conceive)
v. Ovulation inducation with pulsatile GnRH
vi. Laparoscopic drilling (52%, 50%)
vii. IUI +/- ovulation induction with clomiphene or gonadotropins
viii. IVF
ix. GIFT/ZIFT
x. Gestational surrogacy
xi. Donor oocytes

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8
Q

d. What are the long-term sequelae of untreated PCOS? (4)

A

d. Long term sequelae of PCOS:
i. Hirsutism, alopecia and acne
ii. Menstrual bleeding problems
iii. Increased risk of endometrial cancer and hyperplasia
iv. Infertility
v. Increased risk of obesity
vi. Increased risk of diabetes
vii. Increased risk of cardiovascular disease

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9
Q

A patient and her partner have been referred to see you for further management of their infertility. The male partner has azoospermia. The female partner has no abnormalities on investigation.
a. What are the possible causes of azoospermia?

A

a. Causes of azoospermia:
i. Pre-testicular –
a. Kallman syndrome (hypogonadotropic hypogonadism)
ii. Testicular –
a. Genetic (Klinefelter’s syndrome, Y chromosome microdeletions)
b. Congenital (cryptorchidism)
c. Infective (orchitis)
d. Antispermatic agents (heat, irradiation, chemotherapy, drugs)
e. Vascular (torsion, varicocele)
f. Idiopathic
iii. Post-testicular –
a. Obstructive (epidymal – congenital or infection, CBAVD, surgical)
b. Retrograde ejaculation

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10
Q

A patient and her partner have been referred to see you for further management of their infertility. The male partner has azoospermia. The female partner has no abnormalities on investigation.
b. How would you assess this patient?

A

b. Patient assessment –
i. History –
a. Duration of infertility and previous fertility
b. Coital frequency and any sexual dysfunction
c. Childhood illnesses and developmental history
d. Previous surgery or systemic illnesses
e. Previous STIs
f. Exposure to environmental toxins including heat
g. Occupation and use of tobacco, alcohol and other drugs
h. Current medications
ii. Examination:
a. Examination of the penis, including location of the urethral meatus
b. Palpation of the testes and measurement of their size
c. Presence and consistency of the vasa and epididymides
d. Presence of varicocele
e. Secondary sexual characteristics (body habitus, hair distribution, breast development)
f. Digital rectal examination
iii. Investigations:
a. Repeat semen analysis (needs to documented twice)
b. FSH, total testosterone (if testosterone is low repeat to confirm finding and do free testosterone, LH, prolactin
c. USS
d. Karyotype, Y chromosome microdeletions, CF mutation

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11
Q

A patient and her partner have been referred to see you for further management of their infertility. The male partner has azoospermia. The female partner has no abnormalities on investigation.
c. What are the options for the treatment of this couple’s infertility

A

c. Management:
i. Depends on the cause of infertility
ii. Medical
a. Treatment of pituitary adenomas with bromocriptine or cabergoline
b. Treatment of hypogonadotropic hypogonadism unrelated to hypothalamic or pituitary lesions with pulsatile GnRH, hCG or testosterone
iii. IUI +/- ovulation induction
a. Donor or partner sperm
iv. Vasectomy reversal
v. Varicocele repair
vi. IVF and ICSI with testicular sperm extraction

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