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RB Y2 Endocrine - 6 Reproductive > Ovulation Disorders > Flashcards

Ovulation Disorders Flashcards

1
Q

erectile dysfunction in overweight men

A

oestrogen plays a role in fat storing and is naturally present in small amounts in men, when you gain weight, oestrogen levels rise

this inhibits GnRH production and testosterone

results in erectile dysfunction etc

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2
Q

what is the rate limiting step for the production of steroids

A

the conversion of cholesterol to pregnenolone

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3
Q

synthesis of progesterone

A

synthesised from pregnenolone by the action of 3ß-HSD in the corpus luteum, by the placenta during pregnancy and by the adrenals (as a step in the androgen and mineralocorticoid synthesis)

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4
Q

oligomenorrhoea

A

reduction in frequency of periods to less than 9 a year

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5
Q

primary amenorrhoea

A

failure of menarche by the age of 16

think anatomical/congenital (Turner’s/Kallmann) cause?

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6
Q

secondary amenorrhoea

A

cessation of periods for >6 months in an individual who has previously menstruated

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7
Q

physiological causes of amenorrhoea

A

pregnancy

post menopause

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8
Q

causes of secondary amenorrhoea

A

Ovarian problem: PCOS, premature ovarian failure

Uterine problem: uterine adhesions

Hypothalamic dysfunction: weight loss (BMI <18.5), over exercise, stress, infiltrative

Pituitary: high PRL, hypopituitarism

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9
Q

symptoms of oestrogen deficiency

A

flushing, libido, breast tenderness, vaginal atrophy causing dyspareunia (painful sex)

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10
Q

vaginal atrophy

A

inflammation of the vagina due to thinning and shrinking of the tissue

can be due to oestrogen deficinecy

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11
Q

investigations of amenorrhoea

A

LH, FSH, Oestradiol (main oestrogen)

ovarian US ± endometrial thickness

testosterone if there is hirsutism

pituitary function tests and MRI pituitary if indicated

karotype if it is primary amenorrhoea/Turner’s symptoms

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12
Q

what is female hypogonadism identified by

A

low levels of oestrogen

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13
Q

primary hypogonadism

A

problem with ovaries - high FH/LSH = hypergonadotrophic hypogonadism

eg premature ovarian failure

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14
Q

secondary hypogonadism

A

problem with the hyothalamus/pituitary axis - low LH/FSH = hypogonadotrophic hypogonadism

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15
Q

WHO group 1 definition of anovulation

A

hypothalamic pituitary failure

  • low LSH, FH, oestrogen deficiency, normal PRL, amenorrhoea
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16
Q

progesterone challenge test

A

used to evaluate a patient who is experiencing amenorrhoea

progesterone administered as an IM injection

if the patient has sufficient oestradiol, withdrawal bleeding should occur - indicating that the patients amenorrhoea is due to anovulation

if no bleeding occurs it is likely to be due to low serum oestradiol, HPA dysfunction etc

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17
Q

progesterone challenge test in WHO group 1 anovulation

A

negative

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18
Q

WHO group 2 definition of anovulation

A

hypothalamic pituitary dysfunction

  • normal gonadotrophins/excess LH
  • normal eostrogen levels - positive progesterone test
  • oligo/amenorrhoea

PCOS

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19
Q

WHO group 3 definition of anovulation

A

ovarian failure

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20
Q

which WHO group of anovulation is PCOS classified into

A

2

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21
Q

premature ovarian failure

A

amenorrhoea, oestrogen deficiency and elevated gonadotrophins occuring <40 as a result of loss of ovarian function

there is a low likelihood of conception

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22
Q

biochemistry of premature ovarian failure

A

FSH >30 on 2 separate occasions more than one month apart

LH high

oestradiol low

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23
Q

causes of premature ovarian failure

A

autoimmune disease (eg associations with Addison’s, thyroid, APS1/2)

chromosomal abnormalities (e.g. Turner, Fragile X, XX gonadal agenesis)

gene mutations (eg in FSH/LH receptor)

iatrogenic - radio/chemo, bilateral oophorectomy

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24
Q

clinical features of premature ovarian failure

A

features of low oestrogen:

hot flushes

night sweats

atrophic vaginitis

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25
Q

treatment of premature ovarian failure

A

hormone replacement therapy

egg/embryo donation

counselling and support networks

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26
Q

secondary hypogonadism

A

hypogonadism as a result of hypothalamic or pituitary disease

characterised by low oestradiol and low/inappropriately normal LH and FSH

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27
Q

causes of secondary hypogonadism

A

hypothalamic problems:

  • functional disorders: low weight (BMI <18.5), stress, extreme exercise)
  • brain pituitary tumours
  • Kallman’s syndrome
  • IHH

pitutiary problems

miscellaneous: Prader/Willi and haemachromatosis

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28
Q

management of hypothalamic anovulation

A
  • stabilise weight
    • BMI >18.5
  • pulsatile GnRH if hypog hypog
    • -SC/IV, pulsatile administration every 90 minutes
  • LH and FSH daily injections
  • require US monitoring of response
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29
Q

what is the problem with gonadotrophin injections to treat secondary hypogonadism

A

higher multiple pregnancy rates

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30
Q

what is the ovulation rate with pulsatile GnRH treatment for secondary hypogonadism

A

90%

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31
Q

what are the 3 types of functional hypothalamic amenorrhoea

A

weight change

stress

extreme exercise

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32
Q

why does stress cause amenorrhoea

A

evolutionary mechanism to avoid conception during physiological stress

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33
Q

at which BMI does amenorrhoea tend to occur

A

<18.5 normal ovulatory cycle unlikely

<16 cycle usually stops

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34
Q

what happens to GnRH secretion in functional hypothalamic amenorrhoea

A

aberrations in pulsatile GnRH secretion, causes impairement of LH and FSH

there are complex hormonal changes manifested by profound hypooestrogenism

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35
Q

idiopathic hypogonadotrophic hypogonadism

A
  • congenital absent/delayed sexual development associated with inappropriate low levels of gonadotrophic and sex hormones in the absence of anatomical/functional defects of HPA
  • major defect is an inability to activate pulsatile GnRH secretion during puberty due to a genetic defect
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36
Q

what additional phenotype features may be present in IHH

A

anosmia

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37
Q

what mutations have been identified as a cause of IHH

A

mutations in GPCR KISS1R (GPR54) gene

the ligand for KISS1R - ‘Kisspeptin’ is a potent stimulator of GnRH secretion

GnRH neurone has Kisspeptin receptors on it, pulsatile release of Kisspeptin causes pulsatile release of FH and LSH

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38
Q

name 3 functions of Kisspeptin

A

gatekeeper of puberty and GnRH secretion

key regulator of male and female fertility

influence positive and negative feedback of oestrogen and therefore influence ovulation and menstrual cycle

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39
Q

what are most of IHH cases

A

60% kallman’s syndrome

40% normosmic IHH

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40
Q

kallman’s syndrome

A

genetic disorder characterised by loss of GnRH secretion and anosmia/hyposmia

causes primary amenorrhoea

41
Q

why does kallman’s syndrome cause anosmia

A

absence of olfactory bulbs - are in close proximity to the hypothalamus during embryogenesis

42
Q

what is pituitary function and imaging like in kallman’s syndrome

A

remainder of pituitary function normal and MRI imaging normal

43
Q

inheritance of kallman’s syndrome

A

family history

variable patterns of inheritance

genetic heterogenity is displayed (same phenotype casued by different alleles on the same gene)

44
Q

hyperPRL

A

inhibits GnRH secretion

  • can be caused by a prolactinoma or drugs (eg dopamine antagonists)
45
Q

what are some ovarian causes of amenorrhoea

A

ovarian failure (high gonadotrophins)

congenital problem with ovarian development (absence of uterus, vaginal atresia, Turner, CAH)

PCOS

46
Q

PCOS

A

causes secondary oligo/amenorrhoea, infertility, obesity, acne and hirsutism

most common endocrine disorder in women

can be uni or bi lateral

inherited condition

47
Q

what exacerbates PCOS

A

weight

48
Q

diagnosis of PCOS

A

Rotterdam criteria (2/3):

  • menstrual irregularity
  • hyperandrogenism
  • polycystic ovaries
49
Q

what is acanthosis nigricans associated with

A
  • Associated with obesity, insulin resistance, PCOS and adenocarcinoma of the stomach
50
Q

what skin lesion is PCOS associated with

A

acanthosis nigricans

51
Q

blood tests of PCOS

A

increased testosterone (high free androgen)

increased LH:FSH ratio

increased TSH and lipids

impaired glucose tolerance

52
Q

US of PCOS

A
53
Q

insulin resistance in PCOS

A

this is seen in 50-80% of patients

diminshed biological response to a given level of insulin, however as the pancreatic reserve is normal hyperinsulinaemia occurs

20% of patients have glucose intolerance or non-insulin dependent DM

exacerbated by obesity

54
Q

what does hyperinsulinaemia in PCOS result in

A

raised LH levels (altered LH:FSH ratio). This leads to increased androgen synthesis and arrest of normal follicular development

lowered FSH - insufficient to stimulate granulosa cells (infertility?)

lowered SHBG levels, leading to increased free testosterone, leading to hyperandrogenism

55
Q

management of PCOS

A
  1. weight loss and metformin
  2. local measures: shaving, wax, creams etc
  3. OCP - acne and hirsutism respond to this. Can add Crypoterone acetate
  4. cosmesis eg laser phototherapy, electrolysis
56
Q

the risk of which 2 cancers is increased in PCOS

A

ovarian and endometrial

57
Q

OCP action

A

suppresses ovarian androgen production and reduces free androgens by increasing SHBG levels

  • hirsutism benefit and regulates cycles
58
Q

what local anti-androgen creams are available for treatment of PCOS

A

elfornithine cream (Vaniqa) inhibits hair growth

59
Q

what is used in the management of PCOS if the OCP has not been of much benefit

A

cyproterone acetate (steroidal anti-androgen of co-cyprindiol)

often combined with OCP as Dianette

60
Q

use of Metformin in PCOS

A

to restore cycles and fertility, helps insulin resistance and so reduces androgen production

helps all aspects of PCOS

61
Q

what cosmetic management can be performed in PCOS

A

electrolysis and laser phototherapy

62
Q

pre-fertility treatment

A

weight loss to optomise results (BMI >30 has a poor treatment outcome)

lifestyle modifications: smoking and alcohol

folic acid 400mcg daily (5g if BMI >30)

check rubella immune

normal semen analysis

patent fallopian tube

63
Q

what vaccine is given for rubella

A

MMR

(live attenuated vaccine)

UK VACCINATION SCHEDULE: given at 1 year and 3y4m

64
Q

what are the 3 options for ovarian induction in PCOS

A

metformin may induce conception alone

Clomifene citrate

gonadotrophin therapy

laparoscopy ovarian diathermy

65
Q

clomifene citrate (Ovulation Induction in PCOS )

  • possible AE
A

inhibits oestrogen receptors in the hypothalamus, inhibiting negative feedback of oestrogen on gonadotrophin release, leading to up-regulation of HPG axis

may cause ovarian hyperstimulation syndrome

66
Q

gonadotrophin therapy (Ovulation Induction in PCOS )

A

daily injections of recombinant FSH to stimulate the ovary directly

67
Q

what are the risks with gonadotrophin therapy

A

multiple pregnancy and over stimulation

68
Q

laparoscopic ovarian diathermy (Ovulation Induction in PCOS )

A

many singleton pregnancies

69
Q

what is the risk with laparoscopic ovarian diathermy

A

destruction of ovaries

70
Q

what are the risks of ovulation induction

A

ovarian hyperstimulation

multiple pregnancy

ovarian cancer

71
Q

what happens in ovarian hyperstimulation

A
  • Ovaries become swollen and painful. Ovarian enlargement, oedema, hypovolaemia, acute kidney injury
  • Ranges from mild to severe
  • There is an increased risk <35 years, and in PCOS
72
Q

what are the biggest risks in multiple pregnancies

A

prematurity (half of twins are born before 36 weeks) and low birth weight

73
Q

problems associated with prematurity:

A
  • Neonatal intensive care may be required
  • Breathing help
  • RDS
  • Long term: cerebral palsy, impaired sight, congenital heart disease
  • Still birth/neonatal death
  • Disability
74
Q

hirsutism

A

excess hair, usually referring to women with male pattern hair distribution

caused by excess androgen at the hair follicle, due to either excess circulating androgen or increased peripheral conversion at the hair follicle

75
Q

long history causes of hirsutism

A

PCOS, familial (ethnic origin, especially Mediterranean population), idiopathic, CAH

all present with a testosterone that is not dramatically elevated (<5nmol/L) and no virilisation

76
Q

causes of hirsutism with a short history

A

adrenal/ovarian tumour (frequently benign)

high testosterone levels (>5nmol/L), signs of virilisation (deepening of voice and clitoromegaly)

MRI adrenal and ovaries for tumours (>1cm)

77
Q

what can exposure to exogenous testosterone cause

A

hyperandrogenism

78
Q

turner’s syndrome

A

affects women, 45X (one X chromosome missing)

can uncommonly be mosaicism

79
Q

ovarian function in Turner’s syndrome

A

an early loss of ovarian function is common, a small percentage of females will retain normal ovarian function throughout young adulthood

most will be infertile

80
Q

puberty in female’s with Turner’s syndrome

A

most fail to progress through puberty, 30% have some pubertal development

there is normal adrenarche and pubic hair development

breast development depends on when the ovaries fail (there may be none if they fail before puberty)

failure to develop 2y sexual characteristics is typical

81
Q

how does Turner’s present in paediatrics

A

short stature

puberty abnormalities

82
Q

how does Turner’s syndrome present in adults

A

primary or secondary amenorrhoea

infertility

83
Q

clinical features of Turners

A

short stature

webbed neck

shield chest with wide spaced nipples

cubitis valgus

lymphoedema

coarctation of the aorta

84
Q

XX gonadal dysgenesis

A

a form of female hypogonadism, in which there are absent ovaries, without any chromsomal abnormality

85
Q

testicular feminization (androgen insensitivity syndrome)

A

a genetic disorders that makes XY fetuses insensitive to androgen

they are born externally looking like normal girls, and tend to identify with being female

86
Q

define inferility

A

failure to achieve a clinical pregnancy after 12 months or more of regular unprotected sexual intercourse (in absence of known reason) in a couple who have never had a child.

87
Q

define primary and secondary infertility

A
  • primary - the couple have never conceived
  • secondary- the couple have previously conceived (may nothave been successful)
88
Q

list factors that increase the likelihood of conception

A
  • Women <30
  • Previous pregnancy
  • Less than 3 years trying to conceive
  • Intercourse occurring around ovulation
  • Woman’s BMI 18.5 – 30
  • Both partners are non-smokers
  • Caffeine intake of less than 2 cups of coffee daily
  • No use of recreational drugs
89
Q

what drug has a direct correlation to still birth

A

cocaine

90
Q

define anovulatory infertility

A

ovaries do not release an occyte during the menstrual cycle

91
Q

hydrosalpinx

A
  • distally blocked fallopian tube withc lear/serous fluid - may become distended
  • can cause pain, discharge, infertility, menorrhagia and ectopic pregnancy
92
Q

define endometriosis

A

the presence of endometrial glands otuside the uterine cavity

93
Q

most common cause of endometriosis

A

retrograde menstruation - menstrual blood containing endometrial cells flows back out through fallopian tubes into pelvic cavity instead of out of the body

94
Q

classical scan sign of endometriosis

A

chocolate cysts

95
Q

examination of patient for infertility

A
  • BMI
  • general - body hair distribution, galactorrhoea
  • pelvic - presence of vas deferens, varicocele (reduce sperm count)
96
Q

investigation of female for infetility

A
  • Endocervical swab for chlamydia
  • Cervical smear if due
  • Blood for rubella immunity
  • Midluteal progesterone
  • test of tubal patency
97
Q

first line investigation for tubular assessment

A

Hysterosalpingiogram

98
Q

when is laparoscopy first line for infertility

A

known pelvic disease/pathology

RB Y2 Endocrine - 6 Reproductive (4 decks)

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