Infertility Flashcards
List the 8 key features on history that you would want to ascertain for male factor infertility?
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).
list 5 of the parameters in sperm analysis
Volume >1.5ml pH 7.2 motility 40% morphology 4% sperm concentration 15x10^6
what are the baseline hormone investigations you would perform for male factor infertility?
FSH
LH
Testosterone
Prolactin
How does letrozole work?
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
What is the normal letrozole regimen
2.5mg daily on days 2-5 of cycle
monitor with scan mid-cycle
consider a luteal progesterone sample (day 21)
A young married couple have been unable to achieve intercourse, what are the possible causes?
dyspareunia vulvodynia vaginismus vaginitis male impotence psychological social (time, stress, busy, location) FGM lower genetical tract abnormality
What is the treatment for vaginismus?
Physio - myofascial release
Pelvic floor exercises
dilator therapy
sexual therapy
What are the PCOS diagnostic criteria?
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)
List the causes of azospermia
Obstructive endocrine medical iatrogenic chromosomal environmental
List 4 causes of obstructive azospermia?
congenital absence of vas deferens
CF (bilateral congenital absence of vas)
infection/trauma
vasectomy
List 2 endocrine causes of azospermia?
hypogonadotrophic hypogonadism e.g. Kallmans syndrome
Hypergonadotrophic hypogonadism
List 2 medical causes of azospermia
- mumps orchitis
- orchiditis
list 3 iatrogenic causes of azospermia?
- surgical (testicular resection)
- radiation therapy
- chemotherapy
List 2 chromosomal abnormalities associated with azospermia
micro deletions in y chromosome
Klinefelters XXY
How would you approach management for a patient with azospermia?
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
What are the advantages and disadvantages of testicualr extraction to achieve pregnancy?
A - genetics are the fathers
D - cost
- invasive
- require IVF/ICSI
What are the advantages and disadvantages of donor sperm?
IUI can be performed which is cheaper
not genetically father
what is the pathogenesis of OHSS?
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
what are the risk factors for OHSS?
ART PCOS young age previous OHSS hCG administration super-ovulation (>20 follicles /oocytes harvested) high or rapidly increased estradiol
what are the risk factors for OHSS?
ART PCOS young age previous OHSS hCG administration super-ovulation (>20 follicles /oocytes harvested) high or rapidly increased estradiol
Describe management of OHSS
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
Describe management of OHSS
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
Describe management of OHSS
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
what investigations can you do to test for tube patency?
dye test during laparoscopy if no evidence of current infection
HSG
Sonohysterogram
what is the evidence regarding hydrosalpinges and IVF?
Hydrosalpinges reduces overall success rate of IVF
increased live birth with IVF if TL or removal of tubes
List 3 advantages and 3 disadvantages of using hysterosalpingography?
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
what are 2 advantages and disadavantages of hysteroscopy for review of primary infertility
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
What are the advantages and disadvantages of using laparoscopy and dye to assess primary infertility?
A - gold standard for tubal patency, can assess rest of pelvis
D - need GA, does not assess endometrial cavity, surgical risks
Describe the pathophysiology of ovulation
- 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
What is the mechanism whereby a pituitary microadenoma causes anovulation?
- High prolactin
- causes reduced GnRH
- reduced LH/FSH
- no follicle recuitment, low estrogen state
- suppress pituitary
What is the mechanism whereby a pituitary microadenoma causes anovulation?
- High prolactin
- causes reduced GnRH
- reduced LH/FSH
- no follicle recuitment, low estrogen state
- suppress pituitary
What is the mechanism whereby a pituitary micoadenoma causes anovulation?
- High prolactin
- causes reduced GnRH
- reduced LH/FSH
- no follicle recuitment, low estrogen state
- suppress pituitary
what is the mechanism of action of clomiphene?
selective estrogen receptor modulator
competitively blocks estrogen receptors in the hypothalamus
increasing GnRH –> FSH/LH
increasing follicular development
list 5 lifestyle factors that contribute to oligospermia
smoking recreational drugs alcohol obesity high temp environments (riding bike, tight underwear)
List some commonly used drugs that impact or may contribute to oligospermia
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
