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Endocrinology Y2- RDT > endocrine infertility > Flashcards

endocrine infertility Flashcards

1
Q

What is the normal reproductive physiology in males?

A

GnRH stimulates LH and FSH release from APG and they act on Sertoli and Leydig cells in the testis to produce testosterone and inhibin (which then act by negative feedback on the APG).

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2
Q

What is the normal reproductive physiology in females?

A

They have a 28-day menstrual cycle consisting of; follicular phase, ovulation and luteal phase.

High levels of oestradiol trigger a switch to positive feedback on the hypothalamus triggering large GnRH and LH release.

In the luteal phase, if implantation does not occur, the endometrium is shed (menstruation)- if implantation does occur, then pregnancy.

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3
Q

What is the definition of infertility?

A

inability to conceive after 1 year of regular unprotected sex

Affects 1:6 couples

Caused by abnormalities in:

Males- 30%

Females- 45%

Unknown reason- 25%

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4
Q

What are the 2 main reasons for infertility?

A
  1. Primary gonadal failure- gonads fail to high GnRH and LH/FSH but no inhibin/ testosterone (i.e. the gonads cannot function even though they’ve had the right signal)
  2. Hypo/pituitary disease- hypothalamus/ pituitary fail so low FSH/LH and low/ no inhibin/ testosterone etc.
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5
Q

What are the clinical features of hypogonadism in males?

A

Loss of libido = sexual interest / desire

Impotence

Small testes

Decrease muscle bulk

osteoporosis

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6
Q

What are the causes of hypogonadism?

A
  1. Hypothalamic-pituitary disease
  2. Primary gonadal disease
  3. Hyperprolactinaemia
  4. Androgen receptor deficiency
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7
Q

When would hypothalamus-pituitary disease result?

A

Hypopituitarism

Kallmans syndrome (anosmia and low GnRH- hypothalamic issue- occurs in concordance with a lack of smell (olfactory nerves migrate from the GnRH neurones)

Illness/ underweight (low BMI)- hypothalamic amenorrhoea in women occurs if they are underweight.

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8
Q

When would primary gonadal disease result?

A

Congenital- Klinefelter’s syndrome (XXY)

Acquired: testicular torsion, chemotherapy

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9
Q

What investigations would you do when diagnosing hypogonadism in males?

A
  • Measure LH, FSH and testosterone levels- if all are low, then you need to do an MRI of the pituitary (it is likely the default is there)
  • Measure the prolactin (prolactin supresses the release of GnRH)
  • Sperm count (azoospermia- absence of sperm in the ejaculate, oligospermia- reduced sperm in the ejaculate)- should be 6-10 million sperm.
  • Chromosomal analysis- i.e. testing for XXY, Klinefelter’s syndrome
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10
Q

What are the treatment options available for hypogonadism for males?

A
  • HRT- replace testosterone for all patients
  • For fertility, you will also need to supply the gonadotrophins (LH and FSH)- subcutaneous injections to stimulate spermatogenesis in testis.
  • Hyperprolactinaemia- dopamine agonist to reduce prolactin levels (this will reduce the suppression of GnRH)
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11
Q

Where are androgens produced (what are the endogenous sites of production)?

A
  1. interstitial Leydig cells of the testes
  2. adrenal cortex (males and females)
  3. ovaries
  4. placenta
  5. tumours
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12
Q

What are the main actions of testosterone?

A
  1. Development of male genital tract
  2. Secondary sexual characteristics
  3. Maintenance of adult fertility
  4. Anabolic effects (muscle and bone growth)
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13
Q

What can testosterone be converted to?

A

The enzyme 5-alpha reductase converts testosterone to DHT. DHT acts on androgen receptor

Aromatase enzyme acts on testosterone to form 17 beta-oestradiol and acts on the oestrogen receptor

98% of circulating testosterone is protein bound.

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14
Q

What are the clinical uses of testosterone?

A

Testosterone in adulthood will increase

  • lean body mass
  • muscle size and strength
  • bone formation and bone mass (in young men)
  • libido and potency

It will not restore fertility, which requires treatment with gonadotrophins to restore normal spermatogenesis.

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15
Q

What are the fertility disorders in females?

A
  1. Amenorrhoea
  2. Polycystic Ovarian Syndrome (PCOS)
  3. Hyperprolactinaemia- relates to men and women
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16
Q

What is amenorrhoea?

And what is the difference between primary amenorrhoea, secondary amenorrhoea and oligomenorrhoea?

A

The absence of periods

Primary amenorrhoea- failure to begin spontaneous menstruation by the age of 16

Secondary amenorrhoea- absence of menstruation for 3 months in a woman who has previously had cycles.

Cycles, on average is 28 days, normal cycle ranges from 25-35 days.

Oligomenorrhoea- irregular long cycles

17
Q

What are the causes of amenorrhoea?

A
  • Pregnancy/ lactation
  • Ovarian failure- Premature ovarian failure, Ovariectomy, Chemotherapy, Ovarian dysgenesis (Turner’s)- lacking one chromosome (45 XO)
  • Gonadotrophin failure: Hypo/pituitary disease, Kallmann’s syndrome (ansomia, low GnRH), Low BMI- leptin and its effects on reproductive function.
  • Post pill amenorrhoea- the pill contains oestrogen and progesterone. Pituitary gland essentially goes to sleep. Therefore patients need to come off the pill after 4 years and use other forms of protection.
  • Hyperprolactinaemia
  • Androgen excess- gonadal tumour
18
Q

What investigations would you do to diagnose amenorrhoea?

A
  • Pregnancy test
  • LH, FSH and oestradiol levels in blood test- they do vary during the cycle but if they are all very low, then it could indicate hypothalamic disease but otherwise, it is not very useful.
  • Day 21 progesterone- can tell you if the woman ovulated in the previous cycle. Even if you are having regular cycles, does not mean you are losing an egg every cycle.
  • Measure androgens (testosterone and androstenedione)- if they are too high they will switch off periods.
  • Measure prolactin and do thyroid function tests
  • Do chromosomal analysis (turner’s) and do ultrasound scan of ovaries/uterus
19
Q

How do you treat amenorrhoea?

A
  • Treat the cause
  • Primary ovarian failure- infertile (HRT)
  • Hypothalamic/ pituitary disease (HRT for oestrogen replacement and supply gonadotrophins (LH and FSH) for fertility- part of IVF treatment)
20
Q

What is PCOS (poly cystic ovarian syndrome)?

A

Incidence is 1 in 12 women of a reproductive age. Associated with increased cardiovascular risk and insulin resistance.

The eggs in the ovaries do not form fully and they become cysts instead.

21
Q

How do you diagnose PCOS?

A

Diagnosis of PCOS needs 2 of the following things:

  • Polycystic ovaries on ultrasound scans
  • Oligo-/anovulation (irregular or no ovulation)
  • Androgen excess- assessed by clinical examination for hirsutism
22
Q

What are the clinical treaments of PCOS?

A
  • Metformin- insulin sensitizer
  • Clomiphene
  • Gonadotrophin therapy (part of IVF treatment)
23
Q

What is clomiphene?

A

Clomiphene is an anti-oestrogenic drug in the Hypothalamic-Pituitary Axis (oestrogen antagonist). Clomiphene binds to the oestrogen receptors in the hypothalamus and blocks normal negative feedback resulting in an increase in GnRH and gonadotrophin secretion.

24
Q

What is hyperprolactinaemia?

A

When you have too much prolactin

25
Q

What are the causes of hyperprolactinaemia?

A
  • Dopamine antagonist drugs (anti-emetics (metoclopramide) and anti-psychotics (phenothiazines))
  • Prolactinoma
  • Stalk compression due to pituitary adenoma. Stalk compression may stop dopamine and TRH passing down as there is a majority negative feedback, a compressed stalk allows autonomous output to begin.

prolactin control is done by suppression (i.e. by dopamine)

26
Q

What are the actions of prolactin?

A

Reduce LH actions on gonads and reduce GnRH pulsatility. You need pulsatile GnRH to be fertile.

27
Q

Why would prolactin increase? (i.e. give more reasons)

A

PCOS

Hypothyroidism

Oestrogens (OCP), pregnancy, lactation

Idiopathic

28
Q

What are the clinical features of hyperprolactinaemia?

A
  • Galactorrhoea
  • Reduced GnRH secretion/ LH action
  • Prolactinoma- leading to headache and visual defects
29
Q

What is the treatment of hyperprolactinaemia?

A

TREAT THE CAUSE! - stop the drugs (if you can)

Dopamine agonists- like bromocriptine and cabergoline (this is quite potent and works well)

Prolactinoma- use dopamine agonist therapy and surgery if really required (but is invasive so try and avoid).

Endocrinology Y2- RDT (7 decks)

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