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Endocrinology > Endocrinology of Pregnancy > Flashcards

Endocrinology of Pregnancy Flashcards

1
Q

Hormone associated with the luteal phase?

A

Prgoesterone

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2
Q

Rise in which hormone causes ovulation?

A

LH

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3
Q

Hormone used in pregnancy test?

A

HCG (human chorionicgonadotropin)

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4
Q

Macrosomia

A

Big baby lol (>4kg)

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5
Q

Polyhydramnios

A

Excess amniotic fluid in the amniotic sac

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6
Q

IGUR

A

Intra-uterine growth retardation

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7
Q

Complications in neonates related to GD

A

Respiratory distress- immature lungs
Hypoglycaemia- fits
Hyperglycaemia- fits

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8
Q

Complications in pregnancy related to GD

A 
Congenital malformation
IUGR (intra-uterine growth retardation)
Macrosomia
Prematurity
Polyhydroamnios
Intrauterine death
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9
Q

In which trimester does the baby produce its own insulin?

A

The third trimester. The insulin is a MAJOR growth factor

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10
Q

Medication you can use during pregnancy to control blood pressure

A

Labetalol
Nifedipine
Methyl dopa
AVOID ACEi AND STATIN

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11
Q

Management of gestational diabetes

A

Pre-pregnancy Counseling - good sugar control pre conception - limit risk of congenital malformation
Folic Acid 5mg
Consider change from tablets to insulin
Regular eye checks - accelerated retinopathy
Avoid ACEI, Statin - for BP use Labetalol, Nifedipine, methyl dopa

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12
Q

Blood sugar level aims pre and post meal

A

<7-8 2 hours post meal

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13
Q

How could you maintain good blood glucose levels during labour?

A

IV dextrose and IV insulin

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14
Q

Which type of diabetes may you develop later in life after pregnancy?

A

Type 2

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15
Q

Which trimester is gestational diabetes most likely to arise?

A

Third trimester

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16
Q

Hyperemesis gravidarum

A

Complication of pregnancy, vomitting, nausea and dehydration (Kate Middleton had it)

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17
Q

Oligomenorrhea

A

reduction in frequency of periods to less than 9/year

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18
Q

Primary amenorrea

A

Failure of menarche by age 16

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19
Q

Secondary amenorrea

A

cessation of periods for >6 months in an individual who has previously menstruated

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20
Q

Causes of primary amenorrea?

A

Consider congenital conditions, e.g. Kallman, Turner’s syndrome

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21
Q

Causes of secondary amenorrea?

A

Ovarian problem: PCOS, Premature Ovarian Failure
Uterine problem: uterine adhesions
Hypothalamic Dysfunction: weight loss, over exercise, stress, infiltrative
Pituitary: high PRL, hypopituitarism

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22
Q

What produces progesterone?

A

Corpus luteum

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23
Q

Does estradiol peak before or after ovulation?

A

Peaks before

Progesterone peaks after ovulation

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24
Q

Investigation for amenorrhea

A

All patients with oligo/amenorrhea
LH, FSH, Oestradiol
Thyroid function, Prolactin

Additional Investigation
Ovarian ultrasound +/- endometrial thickness
Testosterone if hirsutism
Pituitary function tests + MRI pituitary if hypothalamic pituitary probems suspected
Karyotype if primary amenorrhea or features of Turner’s syndrome

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25
Q

Rotterdam criteria for PCOS

A

At least 2 of:

  • Polycistic ovaries (12/more 2-9mm follicles)
  • Oligo/amenorrhea
  • Clinical/biochemical signs of hyperandrogenism (acne, hirsutism)
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26
Q

Role of metformin in ovulation induction?

A

Along with lifestyle modifications
Improves insulin resistance, reduction in androgen production
Restoration of menstruation and ovulation
Does not help in weight loss
May increase in pregnancy rate
?Better response to clomifene or OI following pre-treatment with Metformin

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27
Q

Signs of reduced ovarian reserve?

A

Raised FSH
Low anti-mullerein hormone
Reduced antral ovarian follicle count on USS

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28
Q

Management of reduced ovarian reserve?

A
  • Assisted conception treatment
  • Outcome poor
  • May need donor eggs
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29
Q

History taking for hyperprolactinemia?

A
  • Amenorrhea
  • Galactorrhea
  • Current medication
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30
Q

Premature Ovarian Failure?

A
  • Menopause before age 40

- Raised FSH (>3IU/L x2 samples, low oestrogen levels)

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31
Q

Management for Premature Ovarian Therapy

A
  • Egg or embryo donation
  • Ovary/egg/embryo cryopreservation prior to chemo/radiotherapy where premature ovarian failure anticipated
  • Counselling/support network
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32
Q

Medical treatment for hyperprolactinemia?

A

-Cabergoline twice weekly
-Bromocriptine
(should be stopped when pregnancy occurs)

33
Q

Ovarian Hyperstilmulation?

A

Ovarian hyperstimulation syndrome (OHSS) is an acute inflammatory condition with elevated levels of C-reactive protein (CRP).[2]
The ovaries may form 20 follicles or more and swell following an increase in serum levels of hCG. This results in very high levels of oestrogen production.
It may be classified as mild, moderate or severe (see under ‘Classification’, below) and severe cases can be life-threatening.

Classification

Mild OHSS
Abdominal bloating.
Mild abdominal pain.
Ovarian size usually ‹8 cm*.

Moderate OHSS	
Moderate abdominal pain.
Nausea ± vomiting.
Ultrasound evidence of ascites.
Ovarian size usually 8-12 cm*.
Severe OHSS	
Clinical ascites (occasionally hydrothorax).
Oliguria.
Haemoconcentration haematocrit ›45%.
Hypoproteinaemia.
Ovarian size usually ›12 cm*.
Critical OHSS	
Tense ascites or large hydrothorax.
Haematocrit ›55%.
White cell count ›25 x 109/L.
Oligo-anuria.
34
Q

Risks of ovulation induction?

A

Ovarian hyperstimulation
Multiple pregnancy
??Ovarian cancer

35
Q

When does Oogenesis begin?

A

It begins in utero. It takes many years to complete. It is suspended for several years and then begins again at puberty. It then ceases at menopause.

36
Q

Female Germ Cells

A

Primordial germ cell
-Earliest recognisable germinal cell
-Capable of mitosis
-Migrate to genital ridge by week 6 of embryo development
Oogonia
-Completion of last pre-meiotic division  oocytes
Oocytes enter meiosis
-Primary oocytes - 1st meiotic division
-Secondary oocytes – 2nd meiotic division

37
Q

What forms after the last pre-meiotic division?

A

Oogonia

38
Q

What does the presence of two polar bodies signify?

A

Presence of two polar bodies signifies sperm entry and the completion of 2nd meiotic division.

39
Q

Roughly how many germ cells will be ovulated?

A

400-500 (this is funny cause you have like 400,000 at puberty)

40
Q

Luteal Phase

A

2nd half of cycle
Development of corpus luteum.
Induces preparation of reproductive tract for pregnancy (if fertilisation occurs)

41
Q

What do you call a primary oocyte surrounded by a single layer of granulosa cells?

A

A primary follicle.

Each follicle is capable of producing a single ovum

42
Q

What do the granulosa cells secrete after ovulation?

A

Progesterone

43
Q

How does the follicular phase end?

A

With ovulation

44
Q

Which hormones are secreted in the follicular/luteal phase?

A

Oestrogen secreted in the follicular phase

Progesterone secreted in the luteal phase

45
Q

What happens to the follicular cells left behind after ovulation?

A

They undergo luteinisation and form the corpus luteum

46
Q

What does degeneration of the corpus luteum signify?

A

Signifies start of new follicular phase

47
Q

FSH and LH stimulate secretion of which hormone?

A

Oestradiol

48
Q

What does oestradiol do?

A

Stimualtes release of egg and thickening of uterus lining

It is the strongest acting of the 3 naturally occuring oestrogens.

49
Q

FSH

A

Acts on ovary
Stimulates development of follicles
FSH + LH stimulate secretion of oestradiol and ovulation

50
Q

LH

A

Acts on ovary

Stimulates follicle maturation, ovulation and development of the corpus luteum

51
Q

What do the theca cells produce?

A

They produce androgen.

Androgen is converted to oestradiol by granulosa aromatase

52
Q

Investigations of amenorrhea if hypothalamic pituitary problem suspected?

A

Pituitary function tests and MRI pituitary

53
Q

How is female hypogonadism identified?

A

Low levels of oestrogen

54
Q

Which autoimmune disorders may be associated with premature ovarian failure?

A

Addisons, Thyroid (Hashimotos), APS1/2 (autoimmune polyendocrine syndrome)
Also heart disease

55
Q

Test for premature ovarian failure

A

FSH>40 on 2 separate occasions more than 1 month apart

56
Q

Premature ovarian failure triad

A

Amenorrhea
Hypergonadism
Hypoestrogenism

57
Q

Causes of premature ovarian failure

A
  • Chromosomal abnormalities (e.g. Turner’s syndrome, Fragile X)
  • Gene mutations (e.g. FSH receptor/LH receptor)
  • Autoimmune disease (e.g. association with Addison’s, thyroid, APS1/2)
  • Iatrogenic (radiotherapy/chemotherapy)
58
Q

What type of hypogonadism could Prader Willi syndrome / Haemochromatosis cause?

A

Secondary hypogonadism

59
Q

Is Kallman’s more likely to affect men or women?

A

Men:women 4:1
May be associated with a family history and shows variable patterns of inhertience
Genetic heterogenity

60
Q

Genetic heterogenity definition

A

Phenomen in which a single phenotype or genetic disorder may be caused by any one of a multiple number of alleles e.g. Kallmans

61
Q

Pituitary MRI in Kallmann syndrome

A

Normal MRI

62
Q

PCOS criteria

A

Rotterdam criteria: 2 of:
Menstrual irregularity
Hyperandrogenism (hirsutism, elevated free testosterone)
Polycystic ovaries

63
Q

When 21-hydroxylase doesn’t work, what might happen?

A

Excess testosterone->hirsutism

64
Q

Most common cause of hirsutism?

A

PCOS

65
Q

Congenital adrenal hyperplasia mode of inheritance

A

Autosomal recessive

-Varied clinical presentation

66
Q

Presentation of non-classic CAH?

A

Usually presents in adolescence with hirsutism, menstrual problems, infertility due to anovulation

67
Q

A deficiency in which enzyme is responsible for CAH?

A

21 alpha hydroxylase

68
Q

There is increased production of which compound in CAH (ESPECIALLY after synachten test)?

A

17-OH Progesterone

69
Q

17- OH progesterone and CAH?

A

Increased production of 17-OH progesterone in CAH because enzyme isn’t there to convert it otherwise (enzyme deficiency is 21-OH)

70
Q

In which condition, might you see increased 17-OH progesterone? (especially after synachten test?)

A

CAH

71
Q

Treatment for late onset CAH

A

Low dose glucocorticoid to suppress ACTH drive

72
Q

Short stature, low hairline, fold of skin on neck, constriction of aorta, underdeveloped breasts, shield shaped thorax, elbow deformity, rudimentary ovaries, no menstruation, shortened metacarpal 4, small fingernails, brown spots (nevi) on skin, lymphoedema, WHAT CONDITION DOES YO CHILD HAVE?

A

Turner syndrome

73
Q

Turner syndrome clinical features?

A

Short stature
Webbed neck
Shield shaped chest with widely spaced nipples
Cubitus valgus

74
Q

Turner Presentation

A 
Presentation in paediatrics
-Short Stature
-Failure to progress through puberty
-Normal adrenarche (pubic hair development)
-Breast development – depends when ovaries fail.  May -have no breast development
-30% have some pubertal development
Presentation in adults
-Primary or secondary amenorrhea
-Infertility
75
Q

Do you get pubic hair development in Turner’s?

A

yeah

76
Q

XX gonadal dysgenesis

A

absent ovaries but no chromosomal abnormality

77
Q

Testicular Feminisation

A

Androgen insensitivity syndrome. Genetically XY Male (with testes), but in the complete form, phenotypically female (pseudohermaphrodites)

78
Q

Symptoms of Hypogonadism

A

For men, these symptoms include decreased libido, erectile dysfunction, decreased muscle strength, and diminished aggressiveness and drive. For women, symptoms include amenorrhea and dyspareunia.

Endocrinology (30 decks)

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