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Year 2- ENDO mine > endocrine infertility > Flashcards

endocrine infertility Flashcards

1
Q

describe the male hypothalamo-pituitary-gonadal axis

A
  • GnRH pulses from the hypothalamus
  • stimulates the release of LH and FSH from the pituitary
  • LH then stimulates testosterone production in the testes (Leydig cells)
  • testosterone is then responsible for the secondary sexual characteristics and aids spermatogenesis
  • FSH stimulates Sertoli cells in seminiferous tubules -> sperm and inhibin A and B
  • inhibin has a negative feedback on pituitary FSH secretion
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2
Q

what are the three phases in the female menstrual cycle?

A

follicular phase
ovulation
luteal phase

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3
Q

how long does the female menstrual cycle last?

A

28 days

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4
Q

what happens in the luteal phase?

A

If implantation does NOT occur –endometrium is shed (menstruation)

If implantation DOES occur > pregnancy

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5
Q

define infertility

A

Infertility: inability to conceive after 1 year of regular unprotected sex.

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6
Q

describe the hypothalamo-pituitary-gonadal axis
Female
follicular phase

A
  • LH stimulates production of oestradiol and progesterone in the ovaries
  • FSH stimulates follicular development and inhibin
  • by around day 10, the leading follicle develops into a graffian follicle
  • oestrogen initially negatively inhibits LH and FSH secretion
  • so in the follicular phase their HPG axis is basically the same as men
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7
Q

describe the hypothalamo-pituitary-gonadal axis
Female
luteal phase

A
  • once the oestrogen levels reach a certain point it switches from negative to positive feedback
  • it increases GnRH release and increases LH sensitivity to GnRH
  • this leads to mid-cycle LH surge
  • this triggers ovulation from the leading follicle
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8
Q

what is primary gonadal failure?

A
  • this is a defect of the gonads
  • the testes or ovaries are not producing testosterone/oestrogen so there is no negative feedback on the HPG axis meaning that you can get high GnRH and High LH and FSH
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9
Q

what is hypothalamic/pituitary disease?

A

this is caused by an inability of the pituitary gland to produce FSH and LH so their levels are low
as a result you also have low oestradiol/testosterone

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10
Q

Male Hypogonadism - clinical features

A 
Loss of libido = sexual interest / desire
Impotence 
Small testes
Decrease muscle bulk
osteoporosis
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11
Q

what are the causes behind male hypogonadism?

A

Hypothalamic-pituitary disease

  • Hypopituitarism
  • Kallmans syndrome (anosmia & low GnRH)
  • Illness/underweight (mainly due to the low levels of leptin)

primary gonadal disease (congenital: klinefelters syndrome, acquired: testicular torsion, chemo)

hyperprolactinaemia

androgen receptor deficiency

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12
Q

what is kallman’s syndrome?

A

testes originally undescended

stature low-normal

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13
Q

what investigations can you do for male hypogonadism?

A

LH, FSH, testosterone
If all low&raquo_space; MRI pituitary

Prolactin

Sperm count
Azoospermia = absence of sperm in ejaculate
Oligospermia = reduced numbers of sperm in ejaculate (can also look at sperm under the microscope to check their number and motility)

chromosomal analyss (eg for klinefelters XXY)

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14
Q

what would be the treatment for male hypogonadism?

A

Replacement testosterone for all patients(thus increases their muscle bulk and protects against osteoporosis)

For fertility: if hypo / pit disease
-subcutaneous gonadotrophins (LH & FSH) injections

Hyperprolactinaemia – dopamine agonist (dopamine has a negative effect on prolactin release)

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15
Q

what are the endogenous sites of production of androgens?

A
  1. interstitial Leydig cells of the testes
  2. adrenal cortex (males and females)
  3. ovaries
  4. placenta
  5. tumours
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16
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)
17
Q

what happens to the circulating testosterone?

A

-98% protein bound
-in different tissues you get testosterone being converted to other things
-5 alpha reductase converts testosterone to dihydrotestosterone (DHT)which then acts on androgen receptors
-aromatase can convert testosterone into 17b-Oestradiol (E2) acts via the oestrogen
receptor (ER)-
e.g. brain and adipose tissue

**DHT and E2 act via the nuclear receptors so they are intracellular and have to go into the nucleus to have an effect

18
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.

19
Q

what fertility disorders can you get in females?

A
  1. Amenorrhoea
  2. Polycystic Ovarian Syndrome (PCOS)
  3. Hyperprolactinaemia
20
Q

what is amenorrhoea?

A

Amenorrhoea = absence of periods

21
Q

what are the different types of amenorrhoea?

A

Primary amenorrhoea = failure to begin spontaneous menstruation by age 16 years

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

Oligomenorrhoea = irregular long cycles

22
Q

what are the potential causes of amenorrhoea?

A

Pregnancy ! / Lactation

Ovarian failure:

  • premature ovarian sufficiency
  • Ovariectomy / chemotherapy
  • ovarian dysgenesis (Turners 45 XO) – lacking one chromosome

Gonadotrophin failure:

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

Hyperprolactinaemia

Androgen excess: gonadal tumour

23
Q

what are the features of turners syndrome?

A

short stature
cubitus valgus (wide carrying angle of the forearm)
gonadal dysgenesis
1:5000 live F births

24
Q

what investigations can you do for amenorrhoea?

A

Pregnancy test

LH, FSH, oestradiol

Day 21 progesterone (there should be a rise to show that they are ovulating)

Prolactin, thyroid function tests (hyper and hypo can cause problems with periods)

Androgens (testosterone, androstenedione, DHEAS)

Chromosomal analysis (Turners 45 XO)

Ultrasound scan ovaries / uterus

25
Q

treatment of amenorrhoea

A

Treat the cause (eg low weight)

Primary ovarian insufficiency – infertile, HRT

Hypothalamic / pituitary disease
HRT for oestrogen replacement
Fertility: Gonadotrophins (LH & FSH) – part of IVF treatment

26
Q

what is PCOS?

what conditions is it associated with?

A

= Polycystic ovarian syndrome

Incidence: 1 in 12 women of reproductive age

Associated with increased cardiovascular risk and insulin resistance (>diabetes) ? why

27
Q

what is the criteria for a PCOS diagnosis?

A

Need 2 of the following:

polycystic ovaries on USS
oligo- / anovulation
clinical / biochemical androgen excess (eg increased growth of hair in a male pattern)

28
Q

what are the clinical features of PCOS?

A

Hirsuitism

Menstrual cycle disturbance

Increased BMI

29
Q

what is the treatment for PCOS?

A

Metformin (insulin sensitiser used in type II diabetes)

Clomiphene

Gonadotrophin therapy as part of IVF treatment

30
Q

what does clomiphene do?

A

It is a fertility drug

Is anti-oestrogenic in the hypothalamo-pituitary axis

Bind to oestrogen receptors in the hypothalamus thereby blocking the normal negative feedback, resulting in an increase in the secretion of GnRH and gonadotrophins
This is used in short periods to kick start the HPG axis

31
Q

what happens in hyperprolactinaemia

A

in the case of prolactin, dopamine, which has a negative effect on prolactin release, is the main hypothalamic hormone controlling prolactin release.
TRH has a mild stimulatory effect
Prolactin is needed to stimulate the production of milk in lactating women.
If it becomes dysregulatd it will switch off gonadal function via LH actions on the ovaries and testes.
It also reduces GnRH pulsatility so that it is released basally all the time rather than in regular pulses

32
Q

Hyperprolactinaemia

-what are the causes?

A

Dopamine antagonist drugs
Anti-emetics (metoclopramide)
Anti-psychotics (phenothiazines)

Prolactinoma

Stalk compression due to pituitary adenoma

PCOS

Hypothyroidism

Oestrogens (OCP), pregnancy, lactation,

Idiopathic

33
Q

how does stalk compression cause hyperprolactinaemia?

A

this means that the dopamine can’t get through to inhibit the prolactin release

34
Q

what are the clinical features of hyperprolactinaemia?

A

Galactorrhoea

Reduced GnRH secretion / LH action&raquo_space; hypogonadism

Prolactinoma

  • Headache
  • Visual field defect
35
Q

what are possible treatment options for hyperprolactinaemia?

A

Treat the cause – stop drugs

Dopamine agonist

  • Bromocriptine
  • Cabergoline

Prolactinoma

  • Dopamine agonist therapy
  • Pituitary surgery rarely needed

Year 2- ENDO mine (19 decks)

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