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Year 2 - LCRS - Endocrinology > Endocrinology of Pregnancy > Flashcards

Endocrinology of Pregnancy Flashcards

1
Q

How is semen made?

A
  • first there is a spermatogonium 44XY
  • then primary spermatocytes (both 44XY) -> formed in basal fluid space surrounding seminiferous tubules
  • then secondary spermatocytes (22X or 22Y) -> penetrate between the Sertoli cells, under the influence of Sertoli secretions they develop in to spermatids
  • then spermatids (22X or 22Y)
  • then spermatozoa (22X or 22Y) -> enter seminiferous fluid which is continuously secreted by Sertoli cells
  • tubular fluid is concentrated/reabsorbed through the actions of oestrogen
  • Nutrients (eg fructose) (-> for long journey) & glycoprotein (-> protection from hostile environment that it will encounter) secretion into epididymal fluid (induced by androgens)
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2
Q

What is in semen?

A

Spermatozoa 15-120 million/ml
Seminal fluid 2-5ml

Leucocytes
(potentially viruses e.g. hepatitis B, HIV)

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3
Q

How many sperm reach areas in female reproductive tract in ejaculation?

A

1/100 of spermatozoa in ejaculate enter the cervix
1/10,000 cervix to ovum
Overall 1/million reach ovum

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4
Q

Briefly summarise the male testis-HP axis

A
  • pulsatile GnRH from hypothalamus
  • LH and FSH from anterior pituitary
  • LH acts on Leydig cells in the testis which are important for the production of testosterone and therefore virilisation and are important in spermatogenesis as well
  • FSH acts on Sertoli cells which are responsible for spermatogenesis and also they produce inhibin
  • testosterone and inhibin exert negative feedback on the hypothalamus and on the anterior pituitary
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5
Q

How long does sperm have to travel to reach the Fallopian tube?

A

Travels 100,000 x its length from Testis to Fallopian tube

-> equivalent of SK -> Brighton -> SK for 1.5m human

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6
Q

Where is seminal fluid produced?

A

Small contribution from:
- Epididymis/testis

Mainly from accessory sex glands:

  • Seminal vesicles
  • Prostate
  • Bulbourethral glands
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7
Q

What are the accessory sex glands in males?

A
  • Seminal vesicles
  • Prostate
  • Bulbourethral glands
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8
Q

What is capacitation of sperm?

A

-> achieve fertilising capacity in the female reproductive tract

  1. Loss of glycoprotein ‘coat’
  2. Change in surface membrane characteristics
  3. Develop whiplash movements of tail

Takes place in ionic & proteolytic environment of the Fallopian tube
Oestrogen-dependent
Ca2+-dependent

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9
Q

Acrosome

A
  • organelle that contains enzymes that can break down the ovum outer membrane (zona pellucida)
  • develops in the anterior half of the head of spermatozoa
  • derived from the Golgi apparatus
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10
Q

What happens in people with aromatase deficiency?

A

-> cannot make oestrogen and also have high testosterone

  • high testosterone causes acne, hirsutism etc.
  • low oestrogen causes being tall because epiphyseal growth plate closure requires oestrogen so the epiphysis of bones keep on growing

-> not many cases known

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11
Q

Acrosome reaction

A
  • Sperm binds to ZP3 (= sperm receptor)
  • Ca2+ influx into sperm (stimulated by progesterone (from corpus luteum))
  • Release of hyaluronidase & proteolytic enzymes
    (from acrosome)

-> Spermatozoon penetrates the Zona Pellucida

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12
Q

Where does capacitation occur?

A

In the female reproductive tract (Fallopian tubes)

- dependent on oestrogen and calcium (the oestrogen dependency is why it has to occur in the female reproductive tract)

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13
Q

What is the sperm receptor on the ovum?

A

ZP3

-> sperm binding causes influx of calcium into the sperm (which is stimulated by progesterone from the corpus luteum) Progesterone=pro-gestation -> promotes pregnancy

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14
Q

Zona Pellucida

A
  • outer membrane of ovum
  • glycoprotein layer
  • broken down and penetrated by spermatozoa after binding to ZP3
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15
Q

Polar body

A
  • when female cells divide, they do not divide equally in terms of cytoplasm
  • the polar body is the cell that has a very tiny amount of cytoplasm
  • it ultimately undergoes apoptosis because it cannot maintain itself
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16
Q

Fertilisation

A
  • Occurs within the Fallopian tube
  • Triggers cortical reaction
  • Cortical granules release molecules which degrade Zona Pellucida (e.g. ZP2 & 3)
  • Therefore prevents further sperm binding as no receptors
  • Haploid -> Diploid
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17
Q

How is the binding of further sperm cells prevented at fertilisation?

A
  • cortical granules are released
  • these degrade the zona pellucida and remove receptors
  • further sperm cannot bind without receptors
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18
Q

Development of the conceptus

A
  • Continues to divide as it moves down Fallopian tube to uterus (3-4 days)
  • Receives nutrients from uterine secretions
  • This free-living phase can last for ~ 9-10 days -> then blastocyst implants
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19
Q

What happens to the corpus luteum if pregnancy does or does not occur?

A
  • if pregnancy occurs, the corpus luteum can be maintained by beta-HCG from the placenta
  • if there is no pregnancy, the corpus luteum becomes a corpus albicans and stops producing progesterone
  • you need a source of HCG to maintain the corpus luteum
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20
Q

Implantation

A
  • Attachment phase: outer trophoblast cells contact uterine surface epithelium
    THEN
  • Decidualisation phase : changes in underlying uterine stromal tissue (within a few hours) -> changes in endometrium due to progesterone
  • Requires progesterone domination in the presence of oestrogen
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21
Q

What is the difference in terms of dosage between HRT and OCP?

A

HRT has a much lower dose than OCP

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22
Q

When does ovarian cancer tend to occur?

A

After child bearing age

23
Q

What cells make up the blastocyst? What do they end up becoming?

A
  • trophoblast cells make up the outer surface of the blastocyst and later make the placenta
  • inner cell mass cells are found on the inside of the blastocyst and later make up the embryo
24
Q

What mediators are released in the attachment of the blastocyst to the endometrium?

A
  • Leukaemia inhibitory factor (LIF) from endometrial secretory glands (& blastocyst?) stimulates adhesion of blastocyst to endometrial cells
  • Interleukin-11 (IL11) also from endometrial cells is released into uterine fluid, and may be involved
  • Many other molecules involved in process (e.g. HB-EGF)
25
Q

What are the important factors for implantation?

A
  • LIF
  • IL-11
  • Progesterone
26
Q

What are important molecules in attachment?

A
  • LIF
  • IL-11
  • maybe also some other factors
27
Q

What occurs during decidualisation?

A

Endometrial changes due to progesterone

  • Glandular epithelial secretion
  • Glycogen accumulation in stromal cell cytoplasm
  • Growth of capillaries
  • Increased vascular permeability (→oedema)

=> all about getting nutrients to that area

28
Q

What factors are involved in decidualisation?

A
  • IL-11
  • histamine
  • certain prostaglandins
  • TGF-beta (promotes angiogenesis)
29
Q

Which is the first hormone to go up in pregnancy?

A

HCG

  • > maintains corpus luteum
  • > corpus luteum is the source of progesterone and oestrogen
  • > the hCG is acting on LH receptors
30
Q

Which hormones increase in pregnancy?

A
  • hCG
  • human placental lactogen?
  • oestrogen (mainly oestriol)
  • progesterone
31
Q

hCG full name

A

human chorionic gonadotrophin

32
Q

What are the effects of human placental lactogen?

A

-> metabolic

  • promotes insulin resistance in the mother
  • this is thought to promote nutrients going to the baby (higher blood sugar levels)
33
Q

Why does the hCG only rise for some time?

A
  • in the beginning it is there to maintain the corpus luteum and its progesterone (and oestrogen) production
  • at a point (~10w) the placenta takes over O and P production so the hCG can fall again.
34
Q

Progesterone and oestrogen production during pregnancy

A

First 40 days

  • Produced in corpus luteum (in maternal ovary)
  • stimulated by hCG (produced by trophoblasts) which acts on LH receptors
  • Essential for developing fetoplacental unit
  • Inhibits maternal LH & FSH (-ve feedback)

From day 40
- Placenta starts to take over

35
Q

Draw how the hormones in pregnancy change in level throughout the 40w

A
  • hCG rises and declines at about 40d
  • oestrogen and hpl have a similar curve, rising linearly and falling at 40w, slightly higher curve for oestrogen
  • progesterone rises with a higher inclination than oestrogen, falls at 40w
36
Q

Where is hCG secreted from?

A
  • initially from sincitotrophoblasts from the conceptus

- then placenta

37
Q

What does DHEAS stand for?

A

Dehydroepiandrosterone sulfate

38
Q

What is the main source of oestrogens in pregnancy?

A

maternal and foetal DHEAS

Mother: DHEAS -> oestradiol, oestrone
Baby: makes DHEAS -> oestradiol, oestrogen and also makes 16-alpha-hydroxy DHEAS which is turned into oestrus via placenta

39
Q

Prolactin levels in terms of prolactinoma

A
  • increased
  • levels of prolactin indicate how big the tumor is and how, whether it is changing
  • if a woman with a prolactinoma is pregnant you cannot use levels of prolactin as a marker of tumor size any more because of lactotroph hyperplasia -> check visual fields in every trimester
40
Q

Which hormones increase in pregnancy?

A 
ACTH
Adrenal steroids
Prolactin
IGF1 (stimulated by placental GH-variant)
Iodothyronines
PTH related peptides
41
Q

Why do adrenal steroids increase in pregnancy?

A

because of increases in ACTH

42
Q

Why does prolactin increase in pregnancy?

A

lactotroph hyperplasia

43
Q

Why does IGF-1 increase in pregnancy?

A

It is stimulated by placental GH

44
Q

Why do iodothyronines increase in pregnancy?

A

because hCG and TSH share an alpha subunit and therefore the thyroid gland it stimulated to an extent

45
Q

Why are PTH related peptides increased in pregnancy?

A
  • from breast tissue

- increased to mobilise calcium from the mothers skeleton to ensure that there is enough for the foetus.

46
Q

Which hormones decrease in pregnancy?

A
  • gonadotrophin (LH and FSH)
  • pituitary GH
  • TSH
47
Q

Why do gonadotrophins decrease in pregnancy?

A
  • there is high, LH and FSH independent production of oestrogen
  • this oestrogen exerts negative feedback on the H and AP
48
Q

Why is there a decrease in TSH in pregnancy?

A

because hCG does some of its job in terms of stimulating the thyroid gland so there is some more negative feedback to H and AP

49
Q

What are the 3 key hormones in partuition?

A
  • oxytocin
  • oestrogen
  • cortisol
50
Q

What are the main functions of oxytocin?

A
  • Uterine contraction
  • Cervical dilation
  • Milk ejection
51
Q

What are some receptors that kisspeptin neurones have?

A
  • prolactin (fertility problems in hyperprolactinaemia)
  • leptin (fertility problems in anorexia)
  • oestrogen (-ve feedback of O to Hypothalamus)
52
Q

Endocrine control of lactation

A
  • suckling stimulus to nipple
  • neural pathways to the hypothalamus
  • hypothalamus stimulates AP and PP to make prolactin and oxytocin respectively
  • prolactin -> acts on breast tissue for milk production
  • oxytocin -> acts on breast tissue for milk ejection
53
Q

Why may marathon runners get low testosterone or galactorrhoea?

A
  • nipple stimulation activating the axis

- high prolactin causes decreased sex steroid levels.

Year 2 - LCRS - Endocrinology (18 decks)

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