Flashcards in Endocrinology of Pregnancy Deck (78)
Hormone associated with the luteal phase?
Rise in which hormone causes ovulation?
Hormone used in pregnancy test?
HCG (human chorionicgonadotropin)
Big baby lol (>4kg)
Excess amniotic fluid in the amniotic sac
Intra-uterine growth retardation
Complications in neonates related to GD
Respiratory distress- immature lungs
Complications in pregnancy related to GD
IUGR (intra-uterine growth retardation)
In which trimester does the baby produce its own insulin?
The third trimester. The insulin is a MAJOR growth factor
Medication you can use during pregnancy to control blood pressure
AVOID ACEi AND STATIN
Management of gestational diabetes
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
Blood sugar level aims pre and post meal
<7-8 2 hours post meal
How could you maintain good blood glucose levels during labour?
IV dextrose and IV insulin
Which type of diabetes may you develop later in life after pregnancy?
Which trimester is gestational diabetes most likely to arise?
Complication of pregnancy, vomitting, nausea and dehydration (Kate Middleton had it)
reduction in frequency of periods to less than 9/year
Failure of menarche by age 16
cessation of periods for >6 months in an individual who has previously menstruated
Causes of primary amenorrea?
Consider congenital conditions, e.g. Kallman, Turner's syndrome
Causes of secondary amenorrea?
Ovarian problem: PCOS, Premature Ovarian Failure
Uterine problem: uterine adhesions
Hypothalamic Dysfunction: weight loss, over exercise, stress, infiltrative
Pituitary: high PRL, hypopituitarism
What produces progesterone?
Does estradiol peak before or after ovulation?
Progesterone peaks after ovulation
Investigation for amenorrhea
All patients with oligo/amenorrhea
LH, FSH, Oestradiol
Thyroid function, Prolactin
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
Rotterdam criteria for PCOS
At least 2 of:
-Polycistic ovaries (12/more 2-9mm follicles)
-Clinical/biochemical signs of hyperandrogenism (acne, hirsutism)
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
Signs of reduced ovarian reserve?
Low anti-mullerein hormone
Reduced antral ovarian follicle count on USS
Management of reduced ovarian reserve?
-Assisted conception treatment
-May need donor eggs
History taking for hyperprolactinemia?
Premature Ovarian Failure?
-Menopause before age 40
-Raised FSH (>3IU/L x2 samples, low oestrogen levels)
Management for Premature Ovarian Therapy
-Egg or embryo donation
-Ovary/egg/embryo cryopreservation prior to chemo/radiotherapy where premature ovarian failure anticipated
Medical treatment for hyperprolactinemia?
-Cabergoline twice weekly
(should be stopped when pregnancy occurs)
Ovarian hyperstimulation syndrome (OHSS) is an acute inflammatory condition with elevated levels of C-reactive protein (CRP).
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.
Mild abdominal pain.
Ovarian size usually ‹8 cm*.
Moderate abdominal pain.
Nausea ± vomiting.
Ultrasound evidence of ascites.
Ovarian size usually 8-12 cm*.
Clinical ascites (occasionally hydrothorax).
Haemoconcentration haematocrit ›45%.
Ovarian size usually ›12 cm*.
Tense ascites or large hydrothorax.
White cell count ›25 x 109/L.
Risks of ovulation induction?
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.
Female Germ Cells
Primordial germ cell
-Earliest recognisable germinal cell
-Capable of mitosis
-Migrate to genital ridge by week 6 of embryo development
-Completion of last pre-meiotic division oocytes
Oocytes enter meiosis
-Primary oocytes - 1st meiotic division
-Secondary oocytes – 2nd meiotic division
What forms after the last pre-meiotic division?
What does the presence of two polar bodies signify?
Presence of two polar bodies signifies sperm entry and the completion of 2nd meiotic division.
Roughly how many germ cells will be ovulated?
400-500 (this is funny cause you have like 400,000 at puberty)
2nd half of cycle
Development of corpus luteum.
Induces preparation of reproductive tract for pregnancy (if fertilisation occurs)
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
What do the granulosa cells secrete after ovulation?
How does the follicular phase end?
Which hormones are secreted in the follicular/luteal phase?
Oestrogen secreted in the follicular phase
Progesterone secreted in the luteal phase
What happens to the follicular cells left behind after ovulation?
They undergo luteinisation and form the corpus luteum
What does degeneration of the corpus luteum signify?
Signifies start of new follicular phase
FSH and LH stimulate secretion of which hormone?
What does oestradiol do?
Stimualtes release of egg and thickening of uterus lining
It is the strongest acting of the 3 naturally occuring oestrogens.
Acts on ovary
Stimulates development of follicles
FSH + LH stimulate secretion of oestradiol and ovulation
Acts on ovary
Stimulates follicle maturation, ovulation and development of the corpus luteum
What do the theca cells produce?
They produce androgen.
Androgen is converted to oestradiol by granulosa aromatase
Investigations of amenorrhea if hypothalamic pituitary problem suspected?
Pituitary function tests and MRI pituitary
How is female hypogonadism identified?
Low levels of oestrogen
Which autoimmune disorders may be associated with premature ovarian failure?
Addisons, Thyroid (Hashimotos), APS1/2 (autoimmune polyendocrine syndrome)
Also heart disease
Test for premature ovarian failure
FSH>40 on 2 separate occasions more than 1 month apart
Premature ovarian failure triad
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)
What type of hypogonadism could Prader Willi syndrome / Haemochromatosis cause?
Is Kallman's more likely to affect men or women?
May be associated with a family history and shows variable patterns of inhertience
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
Pituitary MRI in Kallmann syndrome
Rotterdam criteria: 2 of:
Hyperandrogenism (hirsutism, elevated free testosterone)
When 21-hydroxylase doesn't work, what might happen?
Most common cause of hirsutism?
Congenital adrenal hyperplasia mode of inheritance
-Varied clinical presentation
Presentation of non-classic CAH?
Usually presents in adolescence with hirsutism, menstrual problems, infertility due to anovulation
A deficiency in which enzyme is responsible for CAH?
21 alpha hydroxylase
There is increased production of which compound in CAH (ESPECIALLY after synachten test)?
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)
In which condition, might you see increased 17-OH progesterone? (especially after synachten test?)
Treatment for late onset CAH
Low dose glucocorticoid to suppress ACTH drive
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 clinical features?
Shield shaped chest with widely spaced nipples
Presentation in paediatrics
-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
Do you get pubic hair development in Turner's?
XX gonadal dysgenesis
absent ovaries but no chromosomal abnormality
Androgen insensitivity syndrome. Genetically XY Male (with testes), but in the complete form, phenotypically female (pseudohermaphrodites)