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MD1 endocrinologie > Les ovaires > Flashcards

Les ovaires Flashcards

1
Q

Location of the ovaries

A

Suspended in the pelvic cavity but their location varies from person to person

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2
Q

Microscopic anatomy of the ovaries (2 sections)

A

Zone médullaire: blood vessels, lymphatic vessels, and innervation

Cortex: follicles, secretion of hormones

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3
Q

What are the two roles of the ovaries?

A

Secrete sex hormones (endocrine)

Produce ovocytes

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4
Q

What are the three phases of the menstrual cycle?

A
  1. Follicular phase
  2. Ovulation
  3. Luteal phase
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5
Q

How does the length of the menstrual cycle vary?

A

Cycle starts on the first day of menstruation

Can last 21-35 days ish

Follicular phase can vary but the luteal phase is mostly always 14 days!

Menstruation typically occurs 14 days before ovulation

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6
Q

What are the phases of the menstrual cycle within the uterus?

A

Proliferative: growing of the endometrium (thickening)

Secretory: the progesterone surge of ovulation ends the proliferative phase, and the endometrium moves into the secretory (or luteal phase) of development –> endometrium moves through an orderly sequence of morphological changes

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7
Q

What are inhibin A and B and how do they follow patterns of progesterone and estrogen secretion?

A

Inhibin A is primarily produced by the dominant follicle and corpus luteum –>, therefore, rises with Progesterone

Inhibin B is predominantly produced by small developing follicles –> therefore, rises with estrogen levels

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8
Q

Negative and positive feedback within the hypothalamic-pituitary-gonadal axis:

A

During most of the cycle, estrogen/progesterone participate in the negative feedback of GnRH and LH/FSH

But before ovulation, estrogen/progesterone participate in positive feedback and help stimulate causing LH to peak around days 12-14

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9
Q

Embryology of the hypothalamus:

A

For the hypothalamus to function properly –> GnRH secretory neurons must migrate to the right place, happens along with olfactory neurons

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10
Q

GnRH

A

Pulsatile, short half-life of 2-4 minutes

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11
Q

What does GnRH pulsatility vary with?

A

Frequence and pulsatility, vary during the cycle which allows for precise secretion of FSH and LH from the pituitary gland at certain moments of the cycle

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12
Q

What happens when GnRH pulsatility is impaired?

A

Fertility is impaired when GnRH pulsatility is inhibited by chronic malnutrition, excessive caloric expenditure, or aging.

A number of reproductive disorders in women with including hypogonadotropic hypogonadism, hypothlamic amenorrhea, hyperprolactinemia and polycystic ovary syndrome (PCOS) are also associated with disruption of the normal pulsatile GnRH secretion

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13
Q

How is the pituitary gland stimulated by the hypothalamus?

A

Depending on the pulsatility of GnRH, LH and FSH secretion will be prioritized

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14
Q

What are the jobs of FSH and LH?

A

FSH: stimulates the maturation of follicles and production of estrogen

LH:

  • Stimulates ovulation (pic essential)
  • Production of androgens by the thèque and
  • Production of progesterone by the corps jaune
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15
Q

How do LH and FSH work during the follicular phase?

A

Theca cell:

LH: contributes indirectly to estradiol production

  • Converts cholesterol to androstenedione which is then transferred directly into the blood or into granulosa cells

Granulosa cell:

FSH: androstenedione –> estradiol

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16
Q

How do LH and FSH work during the luteal phase/during pregnancy?

A

Theca-lutein cells:

  • LH –> Once again converts cholesterol into androstenedione –> blood or transferred into granulosa-lutein cells

Granulosa-lutein cells:

  • LH –> Converts androstenedione into estradiol ​BUT ALSO cholesterol (LDL) into progesterone
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17
Q

What are the three main functions of the ovaries?

A
  1. Follicular maturation through FSH and local peptides
  2. Selection of dominant follicle (process not entirely understood)
  3. Secretion of estrogen by the follicle and of androgens and progesterone
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18
Q

What are the three “phases” of the endometrium?

A

Folliculaire précoce: thin endometrium (after menstruations)

Mi-folliculaire: proliferative endometrium

Lutéale: secretory endometrium

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19
Q

Embryology of germinal cell formation: (4 main times)

A

Primordial germinal cells:

  • At 3-4 weeks, migrate towards “crête génitale” –> mitose –> ovogonies (prémiotiques)

Primary ovocytes:

  • At 10-12 weeks –> meoisis but stops in prophase

Primordial follicles:

  • 16 weeks

Peak number of germinal cells:

  • 20 weeks, 6-7 million cells (1/3 ovogonies and 2/3 primary ovocytes)
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20
Q

Why are you born with 6-7 million follicles but only have around 500 when you are fertile?

A

Growth and atresia in all physiological circumstances and is 100% independent of hormones (depends on local factors)

FSH saves a bunch of follicles

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21
Q

What are primordial follicles?

A

Ovocyte primaire

Couche de cellules folliculaires granulaires aplaties

Mince membrane basale

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22
Q

What are primordial follicles?

A

Ovocyte débute sa croissance, début de zone pellucide

Cellules folliculaire granuleuses deviennent cuboïdales

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23
Q

What are secondary follicles (preantral)?

A
  1. Ovocytes/ovules croissance maximale
  2. Zone pellucide
    • Couche de glycoprotéines, role de protection et conception
  3. Couche granuleuse (granulosa) pluristratifiée
    • Acquisition de récepteurs FSH/estro/androgènes
  4. Thèque du follicule
    • Vascularisation
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24
Q

Start of the follicular phase: FSH

A

Increase in FSH favorises:

  • Growth of a group of follicles vers phase préantrale (follicle secondaire –> tertiaire)
  • Production of estrogen by granular cells (aromatization)
  • Production of FSH and LH receptors in the follicle
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25
Q

Which follicle becomes the dominant one?

A

Dominant one is the one that manages to create a microenvironment dominant in estrogen

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26
Q

Rest of the follicular phase:

A

Estrogen:

  • Locally –> help cells become more granular therefore increase sensitivity to FSH
  • Pituitary –> negative feedback on FSH secretion

FSH:

  • Stimulates the production of Inhibine B which inhibits pituitary release of FSH
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27
Q

What are tertiary follicles? (early antral phase)

A
  1. Ovocyte/ovule in the middle
  2. Pellucid zone
  3. Couche granuleuse (granulosa)
  4. Différenciation du thèque interne et externe
  5. Formation de l’antre
    • Contient des stéroides, protéines, glycoprotéines, cytokines
  6. Cumulus oophorus
  7. Membrane basale entre la thèque et la couche granuleuse
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28
Q

What is a mature follicle?

A

Ready for the ovule to be released

Ovocyte completes it’s meiosis and division

  1. Estrogen levels are at their highest 24-36hrs before ovulation
  2. LH increased 36 hours before and peaks 10-12 hours before ovulation:
    • causes meiosis to finish, synthesis of PGs –> rupture follicle and start progesterone production
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29
Q

What is the corps jaune?

A

Develops from an ovarian follicle during the luteal phase of the menstrual cycle or oestrous cycle, following the release of a oocyte from the follicle during ovulation

–> produces progesterone

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30
Q

What is the luteal phase?

A

14 days and is characterized by:

  1. Luteinization of the follicle –> corps jaune
  2. Production of progesterone and a bit of estrogen
  3. Atresia of the corps jaune –> if b-HCG present, corps jaune will not degrade
  4. Decrease of progesterone and estrogen if no b-HCG –> increase in GnRH which stimulates FSH release towards the end of the cycle
31
Q

What are the main hormones released by the ovaries?

A

All steroid hormones!

  1. Estrogen –> estradiol and estrone
  2. Progesterone
  3. Andregens (DHEA, testosterone, androstenedione)

Their levels vary with the menstrual cycle

Bound to albumin and SHBG –> only about 1% is free

32
Q

What is the purpose of estrogen? (sex, bones, metabolism)

A

Secondary female sexual characteristics:

  • Breasts, OGE, fat distribution, skin, endometrium/vagina, libido

Bones:

  • Decreased reabsorption, closing epiphyses and long bones (growth stopping after puberty)

Metabolic:

  • Inc. HDL, dim. LDL, inc. TG, inc. transport proteins, inc. coagulation
    • CBG increased when on birth control which causes higher levels of total cortisol but not free (there is just more that is bound)
33
Q

What is the purpose of progesterone? (5 main ones)

A
  1. Glandular development: breats and endometrium
  2. Decrease the effects of insulin
  3. Increase in corporal temperation
  4. Increased ventilation
  5. During pregnancy: inhibit lactation, maintain uterus
34
Q

What is the purpose of androgens (testosterone, DHT, androstenedione, DHEA)?

A
  1. Sexual desire
  2. Protein anabolism (skin, muscles, bones)
  3. Hair
  4. Cerebral neurotransmitters
35
Q

How to check if someone is ovulating?

A
  1. Is their cycle regular?
  2. Symptoms (premenstrual, pain, secretions, libido)
  3. Temperature increase?
  4. Progesterone dosage around day 25
  5. Biopsy/echo of the endometrium, follicular echo.
  6. Peak of urinary LH (tests available at pharmacy)
36
Q

How long should it take a couple (who is fertile) trying to get pregnant to actually get pregnant?

A

1 month –> 25%

3 months –> 60%

6 months –> 72%

12 months –> 85%

37
Q

What is the job of ovaries during a women’s life?

A

Childhood: not active

Puberty: activate “axe hypophyso-surrénalien” (adrénarche) and “hypophyso-ovarien” (ménarche)

Fertile period: 400 ovulations

38
Q

What are the first signs of puberty?

A

First clinical signs:

  • Thélarche (70%)
  • Pubarche (30%)

Environ 6 mois entre thélarche et pubarche/adrénarche

Ménarche (12.8 years old) –> 2-2.5 ans après thélarche

39
Q

What are the Tanner stages for public hair?

A

P1 –> absence de pilosité

P2 –> quelques poils longs sur le pubis

P3 –> pilosité pubienne au-dessus de la symphyse

P4 –> pilosité pubienne fournie

P5 –> pilosité s’étend à la racine de la cuisse et s’allonge –> ombillic (garcon)

40
Q

What are the Tanner stages for breasts?

A

S1: absence

S2: petit bourgeon mammaire avec élargissement de l’aréole

S3: glande mammaire dépasse surface de l’aréole

S4: développement maximum du sein –> saillie de l’aréole et du mamelon sur la glande

S5: aspect adulte

41
Q

What is menopause?

A

Happens between 45 and 55 years old

  • Loss of menstruations for 12 months
  • 50% reduction in estradiol secretion
  • FSH increased by x15
  • LH increased by x5
  • Decrease in secretion of progesterone and androgens
42
Q

What is the difference between amenorrhea and oligomenorrhea?

A

Oligomenorrhea: cycle > 35 days, < 9 cycles per year

Amenorrhea: no menstruation

43
Q

Primary vs. secondary amenorrhea:

A

Primary –> has never menstruated

  1. Absence de règle à 13 ans avec l’absence des caractères sexuels secondaires
  2. Absence de règle à 15 ans avec des caractères sexuels secondaires

Secondary: used to have it but it has since stopped

  • 3 months –> if cycles regular, 6 months –> if oligomenorrhea
44
Q

What are the 4 main causes of amenorrhea?

A
  1. Hypothalamic-SNC (GnRH)
    • Hypogonadisme hypo/eugonadotropique
  2. Antéhypophysiaire (LH/FSH)
    • Hypogonadisme hypo/eugonadotropique
  3. Ovarienne
    • Hypogonadisme hypergonadotropique
  4. Utérovaginale
    • Eugonadotropique –> not a hormonal issue
45
Q

What are the most common causes of hypothalamic amenorrhea?

A
  1. Genetic/congenital causes:
    • Isolated GnRH deficit, Kallmann Syndrome (associated with anosmia)
  2. Fonctionnelle:
    • Associated with eating disorders, athletes, chronic illnesses
  3. Anatomical causes:
    • Tumeurs –> Craniopharyngiome
    • Infiltrative –> Sarcoidoise, histiocytose, hemochromatose, lymphome
    • Compression
    • Trauma, hemorrhage, irradiation crânienne
46
Q

What is hypothalamic functional amenorrhea?

A

Quite frequent

Diagnostic d’exclusion

FSH and LH normal or low

TSH, PRL, MRI –> normal

Hypoestrogenism variable depending on the severity

Decreased frequency and amplitude of GnRH secretion (leptin)

47
Q

What are the most common causes of hypothalamic functional amenorrhea?

A

Eating disorders

Severe or prolonged illnesses

Intense physical activity

Stress (CRH)

48
Q

What are the most common causes of pituitary amenorrhea?

A
  1. Genetic/congenital:
    • Deficit in FSH/LH, can be associated with other pituitary deficits, mutations of GnRH/FSH receptors
  2. Endrocine: (most common)
    • HyperPRL (prolactinoma and hypoT4)
  3. Anatomic:
    • Adénomes hypophysaires
    • Tumeurs dans la région hypophysaire
    • Infiltratif/vasculaire (ex: Sheehan)
    • Hypophysite (autoimmune)
49
Q

What are the most common causes of ovarian amenorrhea?

A
  1. Genetic/congenital:
    • Agénésie gonadique
    • Dysgénsie gonadique (ex: Turner)
    • FMR1 (Fragile X permutation), mutation of FSH/LH receptors
  2. Anatomical:
    • Autoimmune –> polyglandular immune syndromes
    • Iatrogenic –> Chimio, radiotx, chx
50
Q

What is dysgénésie gonadique?

A

Malformation of gonads during embryogenesis –> ovarian atrophy

Can cause primary/secondary amenorrhea

Depends on karyotype:

  • Turner Syndrome 45Xo
  • Mosaic (46XX)
  • 47 XXX
51
Q

Turner syndrome:

A

1/2000-5000 female births

45 Xo or Mosaic (45 Xo/46 XX)

Gonadal dysgenesis (fibrous streaks)

Female phenotype

52
Q

Classical presentation Turner syndrome:

A

Small size, primary amenorrhea, no secondary sexual characteristics

  • Cou palmé, oreilles basses, mamelons écartés, ligne de cheveux
  • Petite taille
  • Cubitus valgus, 4e métacarpe court
  • Cardiac/aortic abnormalities, osteoporosis, etc.
53
Q

Amenorrhée utérovaginale: pas de saignement mais estrogen normaux

A

Müllerian anomalies –> trompes, utérus, 2/3 sup. du vagin

Asherman Syndrome

Recurrent endometritis

Syndrôme d’insensibilité aux androgènes

Déficit en 5 alpha-reductase

54
Q

What is the syndrôme d’insensibilité aux androgènes?

A

Karyotype 46XY, feminine phenotype

Y chromosome present –> formation of testicles and secretion of anti-müllerien hormone

Receptors don’t respond to androgens therefore, no masculinization of OGE and no body hair

Primary amenorrhea

55
Q

What is the clinical approach to amenorrhea?

A

Complete hx and e/p

Provera test

B-HCG test

Eliminate common causes: TSH, PRL, FSH (LH and estrogen too)

MRI –> if headaches, visual problems, unexplained hyperPRL, galactorrhea

56
Q

What is the Provera test?

A

10mg PO die x 10 days –> and if bleeding within 10-14 days after = + test

57
Q

Positive Provera test ddx:

A

Tract is normal

  • PCOS
  • Congenital adrenal hyperplasia
  • Cushing and tumours (adrenal/ovarian)

How to differ if primary or central?

  • FSH-LH normal/low –> central
  • FSH-LH high –> primary
58
Q

Negative Provera test ddx:

A

Hypostrogenism –> no endometrium stimulation

Abnormal lower genital tract

59
Q

What is hirsutism?

A

Excessive growth of dark or coarse hair in a male-like pattern — face, chest and back

≥ 8 on the Ferriman-Gallwey scale

60
Q

What is virilization?

A

More severe form of hyperandrogenism

  • Hirstirusm +
    • Clitoromegaly
    • Deeper voice
    • Androgenous alopecia
    • Corporel changes (increased muscle mass, breast shrinkage)
61
Q

What is hypertrichosis?

A

Increased hair growth in “normal” areas

Often associated with medication (ex: antiepileptics)

62
Q

Causes of hirsutism?

A

Interaction between:

  • Circulating levels of androgens
  • Increased follicle sensibility to androgens
  • Higher number of terminal follicles at birth
63
Q

Testosterone in women:

A

Main circulating androgen:

  • 25% from ovaries
  • 25% from adrenal glands
  • 50% from peripheral conversion of androstenedione and DHEA
    • Created in adrenals for the most part
      • Conversion in: liver, skin, adipous tissue
64
Q

DHT in women:

A

Mostly comes from conversion of testosterone (5 alpha-reductase)

  • Principal androgen that works on hair follicles –> stimulates pilosebaceous activity
65
Q

What does an abrupt start of virilization push the dx towards?

A

Ovarian or adrenal tumour

66
Q

What is idiopathic hirsutism?

A

Isolated without any changes to menstrual cycle

67
Q

Diagnostic criteria for PCOS:

A

2/3 of the following:

  1. Hyperandrogenism (clinical or biochemical)
    • Acne, hirsutism, alopecia or high testosterone levels
  2. Oligo-anovulation/infertility
  3. Polycystic ovaries on echo
68
Q

What are the other, less frequent, causes of hirsutism?

A
  1. Medication
  2. Adrenal glands:
    • Congenital adrenal hyperplasia (non-classic forms) –> can mimic PCOS
    • Adrenal tumours
  3. Cushing’s
  4. Ovaraies
    • Hyperthecosis, ovarian tumours, luteoma of pregnancy
  5. RARE: hyperPRL, dysthyroidism, acromegaly
69
Q

How much of the female population has PCOS?

A

5-10% of women, but the variable presentation

70
Q

Pathophysiology of PCOS:

71
Q

Signs of hyperandrogenism:

A

Increases testosterone/DHEAS/androstenedione

Decreased SHBG

Increased LH:FSH (over 3:1)

72
Q

Chronic anovulation/hyperestrogenism:

A

Can lead to hyperplasia/endometrial carcinoma –> therefore test

How to prevent it?

  • Periodic progestatif, birth control

How to treat fertility?

  • Weight loss –> 5-7% in 6 months can restore ovulation in 75% of women
  • Ovulation inductor
  • Metformin
73
Q

Metabolic syndrome associated with PCOS:

A

Increased BMI, waist, BP

Insulin resistance:

  • Hyperinsulinism in younger patients –> Db 2
  • Test in patients –> HbA1c, HGOP 75g, glycémie à jeun

Bilan lipidic (hyperTG, decreased c-HDL, increased c-LDL)

Hepatic steatosis (possible increased hepatic enzymes)

Increased risk of CV disease (longterm)

74
Q

Basis of hirsutism treatment:

A

Oral birth control

Spironolactone

Antiandrogens

Epilation

Rx –> around 3 months to kick in

MD1 endocrinologie (6 decks)

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