Endocrinology > Endocrine Infertility > Flashcards

Endocrine Infertility Flashcards

(44 cards)

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1
Q

Which cells within the testes does LH stimulate and what does it make 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 does it makes these cells produce?

A

Sertoli cells (in the seminiferous tuules) –> they are stimulated to produce sperm and inhibin A and B

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3
Q

What does inhibin inhibit?

A

Pituitary FSH secretion

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4
Q

What are the three phases of the menstrual cycle?

A

Follicular Phase
Ovulation
Luteal Phase

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5
Q

What does LH stimulate in the ovaries?

A

Oestradiol and progesterone production

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6
Q

What does FSH stimulate in the ovaries?

A

Follicular development and inhibin production

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7
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 – inhibits FSH and LH (until a point)

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8
Q

What does the leading follicle develop into by around day 10?

A

Graffian Follicle

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9
Q

Once oestrogen reaches a certain level it switches to positive feedback. How does it do this?

A

It increases the GnRH secretion

It increases LH sensitivity to GnRH

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10
Q

Define infertility.

A

Inability to conceive after 1 year of regular unprotected sex

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11
Q

What is primary gonadal failure and what effects does it have on the HPG axis?

A
  • gonads fail
  • testes/ovaries don’t produce enough testosterone/oestrogen so there is no negative feedback on the HPG axis meaning that you get high GnRH, high LH and high FSH but NO inhibin
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12
Q

Describe the levels of the different hormones in the HPG axis in the case of hypothalamic/pituitary disease causing infertility.

A 
-hypothalamus/pituitary fail so
Low GnRH 
Low FSH 
Low LH 
- and low/no inhibin/testosterone
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13
Q

State some of the clinical features of male hypogonadism.

A 
Loss of libido 
Impotence  
Small testes  
Decreased muscle bulk 
Osteoporosis (testosterone has anabolic action in the bone)
- due to no testosterone
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14
Q

State 5 causes of male hypogonadism.

A
  1. Hypothalamic-pituitary disease
    - Hypopituitarism
    - Kallmans syndrome (anosmia-loss of smell & low GnRH)
    - Illness/underweight (low BMI)
  2. Primary gonadal disease
    - Congenital: Klinefelters syndrome (XXY)
    - Acquired: Testicular torsion- spermatic cord twists, cutting off the blood supply to the testicle, Chemotherapy
  3. Hyperprolactinaemia
  4. Androgen receptor deficiency
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15
Q

State some congenital and acquired causes of primary gonadal disease.

A

Congenital: Klinefelter’s Syndrome (XXY)
Acquired: Testicular torsion, chemotherapy

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16
Q

What are the main investigations for male hypogonadism?

A
  1. LH, FSH and testosterone (if all are low –> MRI to check pituitary problem)
  2. Prolactin
  3. Sperm count (azoospermia – absence of sperm in ejaculate; oligospermia – reduced number of sperm in ejaculate)
  4. Chromosomal analysis (check for Klinefelter’s)
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17
Q

What is given to all patients with hypogonadism?

A

HRT

Testosterone to increase muscle bulk and protect against osteoporosis

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18
Q

How do you restore fertility in someone with hypothalamic/pituitary disease?

Study These Flashcards
A

Subcutaneous gonadotrophin (LH & FSH) injections – stimulates testosterone release

19
Q

What is the treatment for hyperprolactinaemia?

Study These Flashcards
A

Dopamine agonists to inhibit prolactin – bromocriptine and cabergoline

20
Q

State some endogenous sites of production of androgens.

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A
  1. Interstitial leydig cells in the testes
  2. Adrenal cortex
  3. Ovaries
  4. Placenta
  5. Tumours
21
Q

What are the main actions of testosterone?

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A
  1. Development of the male genital tract
  2. Maintains fertility in adulthood
  3. Control of secondary sexual characteristics
  4. Anabolic effects (muscle, bone)
22
Q

Testosterone is heavily plasma protein bound (98% circulating) 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.

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A
  1. Converted by 5-alpha-reductase to dihydrotestosterone (DHT), which acts on androgen receptors (AR)
  2. Converted by aromatase to 17-beta-oestradiol (E2), which acts on oestrogen receptors (OR)
23
Q

What type of receptors does DHT and E2 act on?

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A

Nuclear receptors (as they are steroid hormones)

24
Q

What are the clinical uses of testosterone?

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A 
INCREASES:
1. Lean body mass 
2. Muscle size and strength 
3. Bone formation and bone mass  
4. Libido and potency  
NOTE: it does NOT restore fertility without gonadotrophins
25
What is the difference between primary and secondary amenorrhoea?
Primary Amenorrhoea = failure to develop spontaneous menstruation by the age of 16 years Secondary Amenorrhoea = absence of menstruation for 3 months in a woman who has previously had cycles
26
What is oligomenorrhoea?
Irregular long cycles
27
List some causes of amenorrhoea.
1. Pregnancy/Lactation 2. Ovarian failure: - Premature ovarian insufficiency - Oophorectomy - Chemotherapy - Ovarian dysgenesis (Turner’s Syndrome (45 XO, lacking one chromosome) 3. Gonadotrophin failure: - Hypo / pit disease - Kallmann’s syndrome (anosmia, Low GnRH) - Low BMI - Post pill amenorrhoea 4. Hyperprolactinaemia 5. Androgen excess: gonadal tumour
28
State some features of Turner’s syndrome.
1. Short statue 2. Cubitus valgus (forearm is angled away from the body to a greater degree than normal when fully extended) giving wide carrying angle 3. Gonadal dysgenesis
29
State some investigations for amenorrhoea.
1. Pregnancy test 2. LH, FSH and Oestradiol 3. Day 21 Progesterone (should be high will tell you if woman ovulated in previous cycle) 4. Prolactin 5. Thyroid function test (both hyper- and hypothyroidism can cause problems with the menstrual cycle) 5. Androgens (testosterone, androstenedione, DHEAS) 6. Chromosomal analysis
30
What are the implications on health of polycystic ovarian syndrome (PCOS)?
``` Increased cardiovascular risk Insulin resistance (diabetes) ```
31
What are the criteria for diagnosing PCOS?
They must have at least 2 of the following: 1. Polycystic ovaries on ultrasound scan 2. Clinical/biochemical signs of androgen excess e/g hirsutism 3. Oligoovulation/anovulation (irregular or no ovulation)
32
What are the clinical features of PCOS?
Hirsuitism Menstrual irregularities Increased BMI
33
Describe the treatment for PCOS.
1. METFORMIN – insulin sensitiser 2. CLOMIFENE – oestrogen antagonist, anti-oestrogenic effects in the hypothalamo-pituitary axis – binds to oestrogen receptors in the hypothalamus thereby blocking the negative feedback --> increased GnRH and gonadotrophin secretion GONADOTROPHIN THERAPY as part of IVF treatment
34
What hypothalamic hormone has a stimulatory effect on prolactin release?
Thyrotrophin releasing hormone (TRH)
35
What effect does hyperprolactinaemia have on the HPG axis?
It reduces GnRH pulsatility so that it is released basally all the time rather than in regular pulses It will switch off gonadal function via LH actions on the ovaries and testes
36
State some causes of hyperprolactinaemia.
1. Dopamine antagonists (anti-emetics and anti-psychotics) 2. Prolactinoma 3. Stalk compression due to pituitary adenoma (so dopamine can’t get to adenohypophysis) 4. PCOS 5. Hypothyroidism 6. Oestrogens (OCP), Pregnancy, Lactation Idiopathic
37
What are the clinical features of hyperprolactinaemia?
1. Galactorrhoea 2. Reduced GnRH and gonadotrophin secretion --> HYPOGONADISM 3. Prolactinoma: - Visual field defect - Headache
38
What are the two main reasons for infertility?
1. Primary gonadal failure | 2. Hypo/pituitary disease
39
What proportion of couples will be affected by infertility?
1 in 6
40
What is the treatment for amenorrhoea?
1. Treat the cause (eg low weight) 2. Primary ovarian failure – infertile, HRT 3. Hypothalamic / pituitary disease - HRT for oestrogen replacement - Fertility: Gonadotrophins (LH & FSH) – part of IVF treatment
41
What in the incidence of PCOS?
1 in 12 women at reproductive age
42
What is the treatment of hyperproclactinaemia?
1. Treat the cause – stop drugs 2. Dopamine agonist - Bromocriptine - Cabergoline 3. Prolactinoma - Dopamine agonist therapy - Pituitary surgery rarely needed
43
What is the relationship between dopamine and prolactin?
Dopamine inhibits prolactin
44
What effect does prolactin have on the gonadrotrophins?
Prolactin inhibits GnRH which is required to stimulate production of the gonadotrophins LH and FSH
Endocrinology
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