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Endocrinology Year 2 > Endocrine infertility > Flashcards

Endocrine infertility Flashcards

1
Q

Which cells within the testes does LH stimulate, and what do these cells produce?

A

Leydig Cells

They are stimulated to produce testosterone

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2
Q

Which cells within the testes does FSH stimulate, and what do these cells do?

A 
Sertoli cells (in the seminiferous tubules)
They help in the process of spermastogenesis (by nourishing germs cells), and produce inhibin A and B
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3
Q

What does inhibin do?

A

Inhibits FSH secretion from the anterior pituitary (negative feedback)

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4
Q

What does LH stimulate in the ovaries?

A

Oestradiol and progesterone production

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5
Q

What does FSH stimulate in the ovaries?

A

Follicular development and inhibin production

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6
Q

What effect does oestrogen have on the HPG axis in the follicular phase of the menstrual cycle?

A

It has a negative feedback effect at the level of the hypothalamus and pituitary

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7
Q

What happens right before ovulation when oestradiol reaches a certain level? State the impact of this

A

It switches to having a positive feedback effect at the level of the hypothalamus - increasing GnRH secretion and LH sensitivity to GnRH.

Causes an LH surge necessary for ovulation

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8
Q

Define infertility.

A

Inability to conceive after 1 year of regular unprotected sex

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9
Q

What is primary gonadal failure?

A

It is a problem with the gonads

The testes/ovaries don’t produce enough testosterone/oestradiol => no negative feedback on the HPG axis => high GnRH, high LH and high FSH.

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10
Q

Describe the levels of GnRH, LH and FSH in the case of hypothalamic/pituitary disease causing infertility.

A

Low GnRH
Low FSH
Low LH

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11
Q

State some of the clinical features of male hypogonadism.

A 
Loss of libido 
Impotence 
Small testes 
Decreased muscle bulk 
Osteoporosis
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12
Q

State and catagorise 5 causes of male hypogonadism.

A

Hypothalamic-pituitary failure:

  • Hypopituitarism
  • Kallman’s syndrome (anosmia & low GnRH)
  • Illness
  • Underweight (due low levels of leptin hormone produced by adipose tissue)

Primary gonadal disease:

  • Congenital = Klinefelters syndrome (XXY)
  • Acquired = testicular torsion, Chemotherapy

Hyperprolactinaemia

Androgen receptor deficiency

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13
Q

What are the main investigations that may be carried out for male hypogonadism?

A
  • If LH, FSH and testosterone levels are all low, do an MRI scan to check for a pituitary problem
  • Check prolactin levels
  • Do a sperm count; Azoospermia = absence of sperm in ejaculate
    Oligospermia = reduced numbers of sperm in ejaculate
  • Chromosomal analysis (check for Klinefelters)
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14
Q

What is given to all patients with hypogonadism?

A

Testosterone replacement

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15
Q

How would you treat a patient with secondary hypogonadism who is looking to restore fertility?

A

Subcutaneous gonadotrophin (LH, FSH) injections

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16
Q

What is the treatment for hyperprolactinaemia?

A
  • Dopamine agonists e.g. bromocriptine and cabergoline

- Pituitary surgery (rarely used) if vision is affected by the prolactinoma

17
Q

State some endogenous sites of production of androgens

A
  • Interstitial leydig cells in the testes
  • Adrenal cortex (males and females)
  • Ovaries
  • Placenta
  • Tumours
18
Q

What are the main actions of testosterone?

A
  1. Development of the male genital tract
  2. Maintain fertility in adulthood
  3. Control of secondary sexual characteristics (puberty)
  4. Anabolic effects in muscle and bone
19
Q

Testosterone is heavily plasma protein bound and it can be converted to other hormones in various tissues. State two products that testosterone can be converted to and the enzymes responsible for these conversions.

A
  • Converted by 5-alpha-reductase to dihydrotestosterone (DHT)
  • Converted by aromatase (in brain and adipose tissue) to 17-beta-oestradiol (E2)
20
Q

Name and state the type of receptors that DHT and E2 act on

A

DHT - androgen receptors
E2 - oestrogen receptors

They are Nuclear receptors

21
Q

State the clinical uses of testosterone replacement. What will it NOT do?

A

To increase:

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

It will not restore fertility

22
Q

What is the difference between primary and secondary amenorrhoea? What is oligomenorrhoea?

A

Primary Amenorrhoea = failure to begin spontaneous menstruation by the age of 16 years

Secondary Amenorrhoea = absence of menstruation for 3 months in a woman who has previously had cycles

Oligomenorrhoea = irregular long cycles

23
Q

List some causes of amenorrhoea.

A
  • Pregnancy
  • Lactation
  • Ovarian failure due to premature ovarian insufficiency, ovariectomy/chemotherapy, or ovarian dysgenesis (in Turner’s syndrome)
  • Gonadotrophin failure due to hypo/pit disease, Kallman’s syndrome, low BMI, or post pill amenorrhoea
  • Hyperprolactinaemia
  • Androgen excess due to a gonadal tumour
24
Q

State some investigations that may be carried out for amenorrhoea

A
  • Pregnancy test
  • Measure LH, FSH, oestradiol
  • Measure day 21 progesterone (which should be high to prepare the endometrium for the potential of pregnancy after ovulation)
  • Measure prolactin
  • Thyroid function tests (since hypo/hyperthyroidism affects menstrual cycle)
  • Measure androgens (testosterone, androstenedione, DHEAS)
  • Chromosomal analysis (Turners 45 XO)
  • Ultrasound scan of ovaries/uterus
25
Q

Describe the treatment of amenorrhoea

A

For premature ovarian insufficiency - hormone replacement therapy but they’re infertile

For hypothalamic/pituitary disease - oestrogen replacement therapy and, to restore fertility, give LH and FSH

26
Q

What are the criteria for diagnosing PCOS?

A

They must have at least 2 of the following:

  • Polycystic ovaries on ultrasound scan
  • Clinical/biochemical signs of androgen excess
  • Oligoovulation/anovulation

*1 in 12 women of reproductive age

27
Q

What other problems are associated with PCOS?

A 
Increased risk of cardiovascular disease
Insulin resistance (leading to diabetes)
28
Q

What are the clinical features of PCOS?

A

Hirsuitism
Menstrual cycle irregularities
Increased BMI

29
Q

Describe the treatment for PCOS - what are the functions of the drugs used?

A

METFORMIN – insulin sensitiser

CLOMIFENE – fertility drug that binds to oestrogen receptors in the hypothalamus thereby blocking negative feedback => increased GnRH and gonadotrophin secretion

GONADOTROPHIN THERAPY as part of IVF treatment

30
Q

Which hypothalamic hormone has a stimulatory effect and which has an inhibitory effect on prolactin release?

A

(+) TSH

(-) Dopamine

31
Q

What two effects does hyperprolactinaemia have on the HPG axis?

A
  1. It inhibits GnRH pulsatility (so that it is released at a basal level all the time)
  2. It inhibits LH actions on the ovaries and testes
32
Q

State some causes of hyperprolactinaemia.

A
  • Dopamine antagonist drugs: Anti-emetics against vomiting/nausea (metoclopramide)
    and Anti-psychotics (phenothiazines)
  • Stalk compression due to pituitary adenoma (so dopamine can’t get to adenohypophysis)
  • PCOS
  • Hypothyroidism
  • Oestrogens (OCP)
  • Pregnancy
  • Lactation
  • Idiopathic
33
Q

What are the clinical features of hyperprolactinaemia?

A
  • Galactorrhoea
  • Reduced GnRH and gonadotrophin secretion => HYPOGONADISM
  • Prolactinoma causing visual field defect and/or headache

Endocrinology Year 2 (18 decks)

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