Infertility Flashcards

1
Q

List the 8 key features on history that you would want to ascertain for male factor infertility?

A

1) coital frequency and timing;
2) duration of infertility and previous fertility;
3) childhood illnesses and developmental history;
4) systemic medical illnesses (such as diabetes mellitus and upper respiratory diseases);
5) previous surgery;
6) medications and allergies;
7) sexual history (including sexually transmitted infections); and
8) exposures to gonadotoxins (including environmental and chemical toxins and heat).

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2
Q

list 5 of the parameters in sperm analysis

A

Volume >1.5ml
pH 7.2
motility 40%
morphology 4%
sperm concentration 15x10^6

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3
Q

what are the baseline hormone investigations you would perform for male factor infertility?

A

FSH
LH
Testosterone
Prolactin

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4
Q

How does letrozole work?

A

Letrozole is an aromatase inhibitor
Aromatase is the enzyme responsible for converting products into estrogen
by inhibiting estrogen, letrozole stops the negative feedback that estrogen normally exerts on the hypothalamus

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5
Q

What is the normal letrozole regimen

A

2.5mg daily on days 2-5 of cycle
monitor with scan mid-cycle
consider a luteal progesterone sample (day 21)

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6
Q

A young married couple have been unable to achieve intercourse, what are the possible causes?

A

dyspareunia
vulvodynia
vaginismus
vaginitis
male impotence
psychological
social (time, stress, busy, location)
FGM
lower genetical tract abnormality

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7
Q

What is the treatment for vaginismus?

A

Physio - myofascial release
Pelvic floor exercises
dilator therapy
sexual therapy

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8
Q

What are the PCOS diagnostic criteria?

A

Polycystic ovaries on a scan (20 or more peripheral antral follicles 2-9mm or increased ovarian volume >10cc)
oligomenorrhoea or anovulation
clinical or biochemical signs of hyperandrogegism (acne, hirsutism, male pattern hair loss), (high free testosterone, low SHBG)

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9
Q

List the causes of azospermia

A

Obstructive
endocrine
medical
iatrogenic
chromosomal
environmental

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10
Q

List 4 causes of obstructive azospermia?

A

congenital absence of vas deferens
CF (bilateral congenital absence of vas)
infection/trauma
vasectomy

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11
Q

List 2 endocrine causes of azospermia?

A

hypogonadotrophic hypogonadism e.g. Kallmans syndrome
Hypergonadotrophic hypogonadism

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12
Q

List 2 medical causes of azospermia

A
  • mumps orchitis
  • orchiditis
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13
Q

list 3 iatrogenic causes of azospermia?

A
  • surgical (testicular resection)
  • radiation therapy
  • chemotherapy
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14
Q

List 2 chromosomal abnormalities associated with azospermia

A

micro deletions in y chromosome
Klinefelters XXY

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15
Q

How would you approach management for a patient with azospermia?

A

history
examination
repeat sample (3 months)
serum FSH and testosterone (to discriminate between obstructive and non obstructive i.e. post testicular and pre testicular respectively)
pre-testicular - consider prolactin (hyperprolactinaemia), TFT (hypothyroidism), MRI head (pituitary tumour)
testicular - consider karyotype (klinfelter) and Y chromosome analysis
post -testicular - consider STI screen post ejaculatory urine sample (retrograde ejaculation)
consider testicular biopsy ?sperm retreivable for ICSI

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16
Q

What are the advantages and disadvantages of testicualr extraction to achieve pregnancy?

A

A - genetics are the fathers
D - cost
- invasive
- require IVF/ICSI

17
Q

What are the advantages and disadvantages of donor sperm?

A

IUI can be performed which is cheaper
not genetically father

18
Q

what is the pathogenesis of OHSS?

A

systemic disease caused by hyper stimulated ovaries which produce vasoactive substances e.g. VEGF which increases capillary permeability
vessels become leaky resulting in intra-vascular dehydration and 3rd spacing of fluids
this creates multi organ involvement - pleural effusions, ascites
if pregnancy results then endogenous hCG further contributes to this process

19
Q

what are the risk factors for OHSS?

A

ART
PCOS
young age
previous OHSS
hCG administration
super-ovulation (>20 follicles /oocytes harvested)
high or rapidly increased estradiol

20
Q

Describe management of OHSS

A

classify mild/mod/severe
mod/severe = inpatient
MDT input
daily weight
fluids - treat intravascular depletion with crystalloids up to 2L/day
IDC to monitor fluid balance
daily bloods (electrolytes)
analgesia
VTE prophylaxis
consider ascitic/pleural tap if symptoms require

21
Q

what investigations can you do to test for tube patency?

A

dye test during laparoscopy if no evidence of current infection
HSG
Sonohysterogram

22
Q

what is the evidence regarding hydrosalpinges and IVF?

A

Hydrosalpinges reduces overall success rate of IVF
increased live birth with IVF if TL or removal of tubes

23
Q

List 3 advantages and 3 disadvantages of using hysterosalpingography?

A

A- assess tubal patency, assess endometrial cavity, avoid anaesthetic
D - possible dye allergy, can be painful, perforation still possible, tubal spasm may give false +ve, may miss some endometrial lesions that may be better assessed with hysteroscopy, does not assess rest of peritoneal cavity

24
Q

what are 2 advantages and disadavantages of hysteroscopy for review of primary infertility

A

A - can assess the endometrial cavity, can treat problem while assessing e.g. polyp
D - does not assess tubal patency, risk of GA and risk of perforation

25
Q

What are the advantages and disadvantages of using laparoscopy and dye to assess primary infertility?

A

A - gold standard for tubal patency, can assess rest of pelvis
D - need GA, does not assess endometrial cavity, surgical risks

26
Q

Describe the pathophysiology of ovulation

A
  • pulsatile GnRH release from hypothalamus
  • stimulates production and release of LH and FSH from anterior pituitary
  • FSH stimulates maturation of antral follicles
  • growing follicles secrete estradiol, increases results in a negative feedback onto hypothalamus and anterior pituitary to lower FSH release
  • smaller follicles requires FSH to survive, so they undergo atresia but the largest follicle/s survive.
  • when the primary follicle is mature, the high estradiol switches to positive feedback again and causes a LH surge
  • LH surge activates the oocytes to enter metaphase of meiosis 1 and causes inflammatory response to help follicle burst and release oocyte 36 hrs later (ovulation)
  • corpus luteum secretes progesterone to support endometrium
  • if fertilisation and implantation don’t occur the corpus luteum degenerates due to no hCG, which drops progesterone, which causes endometrium to shed
27
Q

What is the mechanism whereby a pituitary microadenoma causes anovulation?

A
  • High prolactin
  • causes reduced GnRH
  • reduced LH/FSH
  • no follicle recuitment, low estrogen state
  • suppress pituitary
28
Q

What is the mechanism whereby a pituitary micoadenoma causes anovulation?

A
  • High prolactin
  • causes reduced GnRH
  • reduced LH/FSH
  • no follicle recuitment, low estrogen state
  • suppress pituitary
29
Q

what is the mechanism of action of clomiphene?

A

selective estrogen receptor modulator
competitively blocks estrogen receptors in the hypothalamus
increasing GnRH –> FSH/LH
increasing follicular development

30
Q

list 5 lifestyle factors that contribute to oligospermia

A

smoking
recreational drugs
alcohol
obesity
high temp environments (riding bike, tight underwear)

31
Q

List some commonly used drugs that impact or may contribute to oligospermia

A

pre-testicular - affect HPA axis:
anabolic steroids
glucocorticoids
anti-androgens e.g. spironolactone

Direct effect on spermatogenesis:
- anti-fungal ketcoconazole
- chemo
- radiation

post -testicular
- beta blocker
- antidepressants

32
Q

What is the mechanism whereby a pituitary microadenoma causes anovulation?

A
  • High prolactin
  • causes reduced GnRH
  • reduced LH/FSH
  • no follicle recuitment, low estrogen state
  • suppress pituitary
33
Q

Describe management of OHSS

A

classify mild/mod/severe
mod/severe = inpatient
MDT input
daily weight
fluids - treat intravascular depletion with crystalloids up to 2L/day
IDC to monitor fluid balance
daily bloods (electrolytes)
analgesia
VTE prophylaxis
consider ascitic/pleural tap if symptoms require

34
Q

Describe management of OHSS

A

classify mild/mod/severe
mod/severe = inpatient
MDT input
daily weight
fluids - treat intravascular depletion with crystalloids up to 2L/day
IDC to monitor fluid balance
daily bloods (electrolytes)
analgesia
VTE prophylaxis
consider ascitic/pleural tap if symptoms require

35
Q

what are the risk factors for OHSS?

A

ART
PCOS
young age
previous OHSS
hCG administration
super-ovulation (>20 follicles /oocytes harvested)
high or rapidly increased estradiol