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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
Rotterdam criteria for PCOS
At least 2 of: - Polycistic ovaries (12/more 2-9mm follicles) - Oligo/amenorrhea - Clinical/biochemical signs of hyperandrogenism (acne, hirsutism)
26
Role of metformin in ovulation induction?
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
27
Signs of reduced ovarian reserve?
Raised FSH Low anti-mullerein hormone Reduced antral ovarian follicle count on USS
28
Management of reduced ovarian reserve?
- Assisted conception treatment - Outcome poor - May need donor eggs
29
History taking for hyperprolactinemia?
- Amenorrhea - Galactorrhea - Current medication
30
Premature Ovarian Failure?
- Menopause before age 40 | - Raised FSH (>3IU/L x2 samples, low oestrogen levels)
31
Management for Premature Ovarian Therapy
- Egg or embryo donation - Ovary/egg/embryo cryopreservation prior to chemo/radiotherapy where premature ovarian failure anticipated - Counselling/support network
32
Medical treatment for hyperprolactinemia?
-Cabergoline twice weekly -Bromocriptine (should be stopped when pregnancy occurs)
33
Ovarian Hyperstilmulation?
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
Risks of ovulation induction?
Ovarian hyperstimulation Multiple pregnancy ??Ovarian cancer
35
When does Oogenesis begin?
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
Female Germ Cells
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
What forms after the last pre-meiotic division?
Oogonia
38
What does the presence of two polar bodies signify?
Presence of two polar bodies signifies sperm entry and the completion of 2nd meiotic division.
39
Roughly how many germ cells will be ovulated?
400-500 (this is funny cause you have like 400,000 at puberty)
40
Luteal Phase
2nd half of cycle Development of corpus luteum. Induces preparation of reproductive tract for pregnancy (if fertilisation occurs)
41
What do you call a primary oocyte surrounded by a single layer of granulosa cells?
A primary follicle. | Each follicle is capable of producing a single ovum
42
What do the granulosa cells secrete after ovulation?
Progesterone
43
How does the follicular phase end?
With ovulation
44
Which hormones are secreted in the follicular/luteal phase?
Oestrogen secreted in the follicular phase | Progesterone secreted in the luteal phase
45
What happens to the follicular cells left behind after ovulation?
They undergo luteinisation and form the corpus luteum
46
What does degeneration of the corpus luteum signify?
Signifies start of new follicular phase
47
FSH and LH stimulate secretion of which hormone?
Oestradiol
48
What does oestradiol do?
Stimualtes release of egg and thickening of uterus lining | It is the strongest acting of the 3 naturally occuring oestrogens.
49
FSH
Acts on ovary Stimulates development of follicles FSH + LH stimulate secretion of oestradiol and ovulation
50
LH
Acts on ovary | Stimulates follicle maturation, ovulation and development of the corpus luteum
51
What do the theca cells produce?
They produce androgen. | Androgen is converted to oestradiol by granulosa aromatase
52
Investigations of amenorrhea if hypothalamic pituitary problem suspected?
Pituitary function tests and MRI pituitary
53
How is female hypogonadism identified?
Low levels of oestrogen
54
Which autoimmune disorders may be associated with premature ovarian failure?
Addisons, Thyroid (Hashimotos), APS1/2 (autoimmune polyendocrine syndrome) Also heart disease
55
Test for premature ovarian failure
FSH>40 on 2 separate occasions more than 1 month apart
56
Premature ovarian failure triad
Amenorrhea Hypergonadism Hypoestrogenism
57
Causes of premature ovarian failure
- 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
What type of hypogonadism could Prader Willi syndrome / Haemochromatosis cause?
Secondary hypogonadism
59
Is Kallman's more likely to affect men or women?
Men:women 4:1 May be associated with a family history and shows variable patterns of inhertience Genetic heterogenity
60
Genetic heterogenity definition
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
Pituitary MRI in Kallmann syndrome
Normal MRI
62
PCOS criteria
Rotterdam criteria: 2 of: Menstrual irregularity Hyperandrogenism (hirsutism, elevated free testosterone) Polycystic ovaries
63
When 21-hydroxylase doesn't work, what might happen?
Excess testosterone->hirsutism
64
Most common cause of hirsutism?
PCOS
65
Congenital adrenal hyperplasia mode of inheritance
Autosomal recessive | -Varied clinical presentation
66
Presentation of non-classic CAH?
Usually presents in adolescence with hirsutism, menstrual problems, infertility due to anovulation
67
A deficiency in which enzyme is responsible for CAH?
21 alpha hydroxylase
68
There is increased production of which compound in CAH (ESPECIALLY after synachten test)?
17-OH Progesterone
69
17- OH progesterone and CAH?
Increased production of 17-OH progesterone in CAH because enzyme isn't there to convert it otherwise (enzyme deficiency is 21-OH)
70
In which condition, might you see increased 17-OH progesterone? (especially after synachten test?)
CAH
71
Treatment for late onset CAH
Low dose glucocorticoid to suppress ACTH drive
72
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?
Turner syndrome
73
Turner syndrome clinical features?
Short stature Webbed neck Shield shaped chest with widely spaced nipples Cubitus valgus
74
Turner Presentation
``` 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
Do you get pubic hair development in Turner's?
yeah
76
XX gonadal dysgenesis
absent ovaries but no chromosomal abnormality
77
Testicular Feminisation
Androgen insensitivity syndrome. Genetically XY Male (with testes), but in the complete form, phenotypically female (pseudohermaphrodites)
78
Symptoms of Hypogonadism
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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