Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

LCRS Year 2 - Endocrinology > Endocrine Infertility > Flashcards

Endocrine Infertility Flashcards

1
Q

What is are the stimulatory and inhibitory steps in the hypothalamo-pituitary-gonadal axis?

A

Stimulatory

  • Hypothalamus releases GnRH which stimulates pituitary to produce LH/FSH production.
  • LH/FSH stimulate testes to produce testosterone

Inhibitory
- There is negative feedback by testosterone and inhibin on pituitary LH/FSH and hypothalamus GnRH production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How long is the female menstrual cycle, what are the 2 phases and event between them in it?

A

28 days

  • Follicular phase
  • Ovulation
  • Luteal phase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How similar is the hypothalamo-pituitary-gonadal axis in females during follicular phase to males?

A

Almost identical

  • GnRH, LH/FSH all stimulatory resulting in oestradiol and progesterone release
  • Oestradiol + progesterone + inhibin all negative feedback on the pituitary and hypothalamus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How similar is the hypothalamo-pituitary-gonadal axis in females during OVULATION to males?

A

Suddenly different

  • GnRH, LH/FSH still stimulatory
  • But now, oestradiol causes POSITIVE feedback on hypothalamus so GnRH and LH levels surge (FSH rises but nowhere near as much)
  • Needed for egg maturation and ovulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the possible outcomes, based on implantation, of the female luteal phase?

A

If implantation does NOT occur - endometrium is shed (menstruation) and luteal phase ends

If implantation DOES occur - pregnancy and luteal phase continues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the given definition of infertility?

A

The inability to conceive after 1 year of regular unprotected sex (varies depending on who’s writing, can change to 2 years)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How often do couples encounter this problem?

A

1:6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the percentages of the incidence of abnormalities which produce infertility?

A

Males - 30%
Females - 45%
Unknown - 25%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Which hormones are high and low in primary gonadal failure and where has the problem occurred?

A

Low testosterone/oestradiol

High GnRH, LH/FSH

Problem lies in the gonads themselves, unable to produce the end hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Which hormones are high and low in secondary gonadal failure and where has the problem occurred?

A

Low testosterone/oestradiol

Low LH/FSH

Problem with hypothalamus or pituitary

(my personal suspicion is secondary is pituitary problem so you’d have high GnRH but low test/oestr. and low LH/FSH
- tertiary would be hypothalamic failure so everything would be low but the above is what we’ve been told)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the clinical features of male hypogonadism?

A
  • Loss of libido
  • Impotence
  • Small testes
  • Decreased muscle bulk
  • Osteoporosis, testosterone involved usually in bone strength
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the causes of male hypogonadism?

A

Hypothalamic-pituitary disease

  • Hypopituitarism
  • Kallmans syndrome (anosmia (loss of smell), failure to go through puberty and low GnRH, hypothalamus problem)
  • Illness/underweight

Primary gonadal disease

  • Congenital (Klinefelters syndrome (XXY in cells)
  • Acquired (testicular torsion, chemotherapy)

Hyperprolactinaemia

Androgen receptor deficiency (very rare)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Why is anosmia (lack of smell) coincidental with hypogonadism in some cases?

A

GnRH neurones migrate in development from the back of the brain with the smell neurones so if they fail to do this you get low GnRH and a coincident loss in smell, is not a cause of the loss of smell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How is a male investigated for hypogonadism?

A
  • Clinical assessment and history
  • Levels of LH/FSH/testosterone and if all low then MRI scan of the pituitary
  • Prolactin levels
  • Sperm count
  • Chromosomal analysis (Klinefelters XXY)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the terms for results of an abnormal sperm count and what do they mean?

A

Azoospermia = absence of sperm in ejaculate

Oligospermia = reduced numbers of sperm in ejaculate

Euspermia = normal numbers of sperm in ejaculate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the treatment options in cases of male hypogonadism?

A
  • Replacement testosterone (all patients)
  • For fertility if hypo/pit disease - synthetic gonadotrophins (LH/FSH) stimulates sperm and test. production
  • Dopamine agonist in cases of hyperprolactinaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the endogenous sites of production of androgens?

A
  • Interstitial Leydig sites of the testes (testes)
  • Adrenal cortex (M +F)
  • Ovaries
  • Placenta
  • Tumours
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the main actions of testosterone?

A

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

19
Q

What percentage of circulating testosterone is protein-bound?

A

98%

2% free hormone

20
Q

What are the two possible final forms of testosterone after undergoing tissue-specific processing, which hormones convert it to each final form and what type of receptor does each bind to?

A

5alpha-reductase
- converts it to Dihydrotestosterone (DHT) which acts via the androgen receptor (causes androgen effects)

Aromatase
- converts it to 17beta-Oestradiol (E2) which acts via the oestrogen receptor (in brain/adipose tissue)

21
Q

What are the clinical uses of testosterone and what does it NOT do?

A

In adulthood, T will increase:

  • lean body mass
  • muscle size and strength
  • bone formation and bone mass
  • libido and potency

Does NOT restore fertility, requires treatment with gonadotrophins to restore normal spermatogenesis

22
Q

What are the 3 main infertility disorders in women?

A

1) Amenorrhoea
2) Polycystic Ovarian Syndrome (PCOS)
3) Hyperprolactinaemia

23
Q

What does amenorrhoea mean and what are the two types?

A

Absence of periods

Primary and Secondary

24
Q

What is primary amenorrhoea?

A

Failure to begin spontaneous menstruation by age 16 years

25
Q

What is secondary amenorrhoea?

A

Absence of menstruation for 3 months in a woman who has previously cycles?

26
Q

What is oligomenorrhoea?

A

Irregular long menstruation cycles

27
Q

What are the ovarian causes of amenorrhoea?

A 
Pregnancy/Lactation
Ovarian failure
- premature ovarian failure
- ovariectomy/chemotherapy
- ovarian dysgenesis (don't develop) (Turners 45 XO) lacking one chromosome
28
Q

What are 3 features of Turners syndrome (45XO)?

A

Short stature
Wide carrying angle (forearms and wrists)
Gonadal dysgenesis

29
Q

What are hypothalamo/pituitary and other causes of amenorrhea?

A

Gonadotrophin failure

  • Hypo/pit disease
  • Kallman’s syndrome (anosmia, low GnRH)
  • Low BMI
  • Post-pill amenorrhoea

Hyperprolactinaemia

Androgen excess - gonadal tumour

30
Q

What are the 4 main investigations of amenorrhoea to find the cause?

A

In this order

  • Pregnancy test
  • LH, FSH, Oestradiol
  • Day 21 progesterone (will usually have a rise in progesterone around day 21 if they’re ovulating)
  • Prolactin, thyroid function tests
31
Q

What are 3 more ways of investigating the causes of amenorrhoea?

A
  • Androgens (test, androstenedione, DHEAS) (should be low normally)
  • Chromosomal analysis (Turners syndrome 45XO)
  • Ultrasound scan ovaries, uterus
32
Q

How is amenorrhoea treated?

A
  • First treat the cause (e.g. low weight, make them put on weight)
  • Primary ovarian failure - infertile, give HRT for physiological repair
  • Hypothalamic/pituitary disease - HRT for oestrogen replacement, gonadotrophins (LH/FSH) given as part of IVF treatment to reintroduce fertility
33
Q

What is the criteria to diagnose PCOS (polycystic ovarian syndrome)?

A

2 of the following:

  • Polycystic ovaries on ultrasound (ovaries with cysts on)
  • Aligo-/anovulation
  • Clinical/biochemical androgen excess (male hirsute and sexual/physiological features)
34
Q

What are the clinical features of PCOS?

A
  • Hirsutism (male pattern hair growth)
  • Menstrual cycle disturbance
  • Increased BMI
35
Q

How is PCOS treated to restore fertility?

A
  • Metformin
  • Clomiphene
  • Gonadotrophin therapy as part of IVF treatment
36
Q

How does Clomiphene cause its effects?

A
  • Is anti-oestrogenic in the hypothalamo-pituitary axis
  • Binds to oestrogen receptors in hypothalamus thereby blocking the normal negative feedback by oestrogen
  • Results in increase in the secretions of GnRH and gonadotrophins
  • Enhances fertility
37
Q

What are the features of a course of treatment using clomiphene?

A
  • Must be used very carefully
  • Usually a 5 day course
  • Need to make sure you avoid overstimulation
38
Q

How does the hypothalamus control prolactin release?

A

Secretes dopamine which inhibits prolactin release

Secretes TRH which stimulates prolactin release

Dopamine is the main controlling hormone released as the body only requires prolactin to be high in certain circumstances e.g. pregnancy

39
Q

What are the 3 effects prolactin has on the body?

A
  • Stimulates lactation
  • Inhibits GnRH pulsatility
  • Inhibits LH actions on ovary/testes
40
Q

What drugs and tumours can cause hyperprolactinaemia?

A

Dopamine antagonist drugs

  • metoclopramide (anti-emetic)
  • phenothiazines (anti-psychotic)

Prolactinoma - benign tumour producing prolactin

Stalk compression due to pituitary adenoma - no dopamine inhibitory effect

41
Q

What are causes, other than drugs and tumours, of hyperprolactinaemia?

A
  • PCOS
  • Hypothyroidism
  • Oestrogens (OCP, oral contraceptive pill), pregnancy, lactation
  • Idiopathic
42
Q

What are the clinical features of hyperprolactinaemia?

A
  • Galactorrhoea (excess milk production)
  • Reduced GnRH secretion, reduced LH action leading to hypogonadism (due to actions of high prolactin)
  • Prolactinoma - headache, visual field defect
43
Q

How are cases of hyperprolactinaemia treated?

A

Treat the cause

  • Stop drugs if they’re responsible
  • Dopamine agonist (95% of cases treated successfully with this)
  • Prolactinoma can be shrunk with dopamine agonist and pituitary surgery rarely needed as a result
44
Q

What are 2 examples of dopamine agonists which can be used in treatment of hyperprolactinaemia?

A

Bromocriptine

Cabergoline

LCRS Year 2 - Endocrinology (21 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions