Clinical Management of Pregnancy and Parturition

Question 2

What are the key hormones in the reproductive pathway?

Answer 2

Follicle stimulating hormone (FSH) stimulates follicles to grow and produce oestrogen. Luteinising hormone (LH) acts on thecal cells primarily which produce androgens. Androgens convert to oestrogen, which feeds back to the pituitary and causes ovulation.

Question 3

In what manner is GnRH released?

Answer 3

GnRH is released in a pulsatile manner, which causes pulsatile LH release.

Question 4

What happens if you give continuous GnRH?

Answer 4

Continuous GnRH will eventually suppress LH and FSH. This is used in IVF to control the cycle and growth of multiple follicles without the risk of spontaneous ovulation.

Question 5

What can go wrong with the hypothalamo-pituitary-gonadal axis?

Answer 5

Central pathology can lead to a lack of secretion of LH and FSH, hypothalamic/pituitary disease, gonadal damage, failure of germ cell production, and lack of sex steroid production.

Question 6

How do HPG axis issues present in females?

Answer 6

Issues can present as oligoamenorrhoea, amenorrhoea, infertility, oestrogen deficiency, hirsutism, acne, androgenic alopecia, weight gain/loss, and galactorrhoea.

Question 7

What are the causes of amenorrhoea?

Answer 7

Causes include pregnancy, central causes (hypothalamic, pituitary), ovarian causes (Turner’s syndrome, premature ovarian failure, polycystic ovary syndrome), and miscellaneous causes (thyrotoxicosis, chronic disease).

Question 8

What is hypothalamic amenorrhoea?

Answer 8

Hypothalamic amenorrhoea occurs due to severe marked weight loss, excessive exercise, or bulimia, leading to the pituitary gland stopping its function.

Question 9

What is congenital leptin deficiency?

Answer 9

Congenital leptin deficiency affects the reproductive system by leading to severe obesity, hyperphagia, and hypogonadotropic hypogonadism.

Question 10

What are the main anterior pituitary hormones and their roles?

Answer 10

ACTH regulates the adrenal cortex, TSH regulates thyroid hormones, GH promotes growth, LH/FSH control reproduction, and PRL is involved in breast milk production.

Question 11

What causes physiological hyperprolactinaemia?

Answer 11

Physiological hyperprolactinaemia can be caused by stress, physical or psychological factors, and post-seizure events.

Question 12

What are the clinical features of hyperprolactinaemia?

Answer 12

In premenopausal women, features include hypogonadism, oligo/amenorrhoea, symptoms of estrogen deficiency, and galactorrhoea. In postmenopausal women, features are less apparent.

Question 13

What are the causes of pathological hyperprolactinaemia?

Answer 13

Causes include PRL-secreting pituitary tumours, loss of inhibitory effect from dopamine, pituitary stalk compression, drugs, and hypothyroidism.

Question 14

What does premature ovarian insufficiency usually present with?

Answer 14

Premature ovarian insufficiency typically presents with amenorrhoea, oestrogen deficiency, and elevated LH and FSH levels.

Question 15

What are the causes of premature ovarian insufficiency?

Answer 15

Causes include congenital factors like Turner’s syndrome, autoimmune conditions, iatrogenic causes, and mutations in the FSH receptor.

Question 16

What are the phenotypes of Turner’s syndrome?

Answer 16

Phenotypes include short stature, low hairline, widely spaced nipples, webbed neck, nevi, and small fingernails.

Question 17

How do autoimmune conditions lead to POI?

Answer 17

Autoimmune diseases such as Graves Disease and Addison’s can cause POI, with 2-10% of cases linked to adrenal autoimmunity.

Question 18

What is the mechanism of autoimmune POI?

Answer 18

The mechanism is likely due to inflammatory infiltration of follicles and production of anti-ovarian antibodies, leading to apoptosis and atrophy.

Question 19

What is the link between Fragile X premutation & POI?

Answer 19

1 in 200 females have the genetic change leading to FXPOI, which accounts for about 4-6% of all POI cases in women.

Question 20

What is the management of POI?

Answer 20

Management includes diagnosis via serial FSH and E2 levels, karyotyping, screening for autoimmune diseases, and estrogen replacement therapy.

Question 21

What is Polycystic Ovary Syndrome (PCOS)?

Answer 21

PCOS is the commonest endocrine condition affecting 10% of pre-menopausal women, with an unknown aetiology possibly linked to insulin sensitivity.

Question 22

What is PCOS associated with?

Answer 22

PCOS is associated with oligoamenorrhoea, hirsutism, obesity, infertility, polycystic ovaries on ultrasound, and hyperandrogenism.

Question 23

What happens if you do not protect the endometrium from oestrogen exposure?

Answer 23

Failure to protect the endometrium can lead to endometrial hyperplasia due to unopposed oestrogen exposure.

Question 24

What is the Rotterdam diagnostic criteria for PCOS?

Answer 24

The criteria require 2 out of 3: Oligo-/Amenorrhea, clinical or biochemical signs of hyperandrogenaemia, and polycystic ovaries.

Question 25

What are the clinical features of PCOS?

Answer 25

Features include polycystic ovaries, acanthosis nigricans, insulin resistance, obesity, androgen excess, and anovulation.

Question 26

What is hirsutism?

Answer 26

Hirsutism is male hormone dependent hair growth, categorized by hair growth in areas such as the upper lip, chin, and abdomen.

Question 27

What is androgenic alopecia?

Answer 27

Androgenic alopecia is male-pattern baldness that can also occur in females, indicating hirsutism.

Question 28

What clinical problems arise with pregnant women with PCOS?

Answer 28

Common problems include oligo-/amenorrhea, infertility, and increased risk of gestational diabetes and pregnancy-related hypertension.

Question 29

What risks can OHSS cause in a pregnant woman with PCOS?

Answer 29

OHSS can cause dehydration, ascites, kidney problems, and a high risk of venous thromboembolism.

Question 30

What can be treated in PCOS?

Answer 30

Treatment options include lifestyle changes, medications for insulin resistance, and hormonal therapies.

Question 31

What are the treatments for obesity and oligo/amenorrhea?

Answer 31

Metformin, lifestyle modification, MPA (progesterone) 10 mg od for 10 days every 3 months if no spontaneous bleed. ## Footnote Weight loss pharmacotherapy (avoid pregnancy), bariatric surgery (avoid pregnancy for 2 years).

Question 32

What is the significance of losing 10% of body weight in relation to ovulation?

Answer 32

If you lose 10% of body weight, you can regain ovulation.

Question 33

What are the treatment options for anovulatory infertility?

Answer 33

Metformin => Metformin + Clomiphene or Letrozole => Metformin + IVF.

Question 34

What are the treatments for hirsutism?

Answer 34

Yasmin, Vaniqua cream (can have acne side effects), cosmetic removal, spironolactone.

Question 35

What are the three types of anti-androgenic oral contraceptives?

Answer 35

Dianette, estradiol, drospirenone, cyproterone acetate. ## Footnote Dianette has a 1.5 times risk of venous thromboembolism and is not recommended anymore.

Question 36

What is 21-hydroxylase deficiency?

Answer 36

It causes congenital adrenal hyperplasia and can mimic PCOS.

Question 37

What are the two forms of 21-hydroxylase deficiency?

Answer 37

Classical form (neonatal/infancy presentation) and Non-classical form (childhood/adult presentation).

Question 38

What characterizes the classical form of 21-hydroxylase deficiency?

Answer 38

Adrenal androgen excess leading to virilized females and salt-wasting due to aldosterone deficiency.

Question 39

What characterizes the non-classical form of 21-hydroxylase deficiency?

Answer 39

Premature puberty, hirsutism, and it masquerades as PCOS.

Question 40

What is the pathway disrupted in 21-hydroxylase deficiency?

Answer 40

Can't convert to aldosterone or cortisol, leading to more androgens and testosterone.

Question 41

How do you test for 21-hydroxylase deficiency?

Answer 41

If 17 OHP is high, it indicates 21-hydroxylase deficiency.

Question 42

What is androgen insensitivity syndrome?

Answer 42

A spectrum of disorders due to mutations in the androgen receptor, including complete, incomplete, Reifenstein's, and poorly virilized infertile males.

Question 43

What are the features of someone with complete androgen insensitivity syndrome?

Answer 43

Female external genitalia, short blind-ending vagina, no uterus, abdominal/inguinal testes, absent prostate, axillary (pubic) hair, gynaecomastia.

Question 44

What is the presentation of androgen insensitivity syndrome?

Answer 44

Inguinal hernia, primary amenorrhea, elevated LH, testosterone, and E2 in bloods.

Question 45

What is 5a-reductase deficiency?

Answer 45

Inability to convert testosterone to DHT, leading to lack of virilization of external genitalia.

Question 46

What are the key principles governing male reproduction?

Answer 46

Negative feedback, LH vs FSH drive, testosterone production by Leydig cells.

Question 47

How does hypogonadism present in males?

Answer 47

Delayed puberty, psychological effects, loss of libido, erectile impotence, gynaecomastia, loss of body hair, decreased muscle mass, osteoporosis, infertility.

Question 48

How do you measure testis size?

Answer 48

Use an orchidometer to measure size in ml.

Question 49

What are the causes of primary hypogonadism in males?

Answer 49

Trauma, chemotherapy, undescended testes, infections, chromosomal abnormalities, systemic diseases.

Question 50

What are the causes of secondary hypogonadism in males?

Answer 50

Pituitary tumors, hyperprolactinemia, hypothalamic disorders, systemic disease, androgen use.

Question 51

How is hypogonadism investigated?

Answer 51

Clinical examination, LH, FSH, testosterone levels, further investigations based on results.

Question 52

What is Klinefelter's syndrome?

Answer 52

Affects 1:1000 males, characterized by a 47 XXY karyotype and primary hypogonadism.

Question 53

What is myotonic dystrophy?

Answer 53

An autosomal dominant disorder causing progressive muscular weakness, myotonia, and primary gonadal failure.

Question 54

What is Kallman's syndrome?

Answer 54

Idiopathic hypogonadotropic hypogonadism with anosmia in 75% of cases.

Question 55

What are the genetic defects of hypogonadotropic hypogonadism?

Answer 55

Mutations in Kal-1, FGF-Receptor 1, prokineticin, GnRH-Receptor, and G-protein coupled receptor 54.

Question 56

How can testosterone be replaced and what are the risks?

Answer 56

Injections, transdermal patches, or subdermal implants. Risks include aggressive behavior, prostate cancer, and infertility.

Question 57

What is androgen abuse and its hazards?

Answer 57

Designer drugs that increase testosterone, leading to psychological changes, hypogonadism, prostate cancer, and cardiovascular issues.

Question 58

What are the causes, assessment, and diagnostics of male infertility?

Answer 58

Assessment includes history, examination, seminal fluid analysis, and hormone levels. Treatment may involve replacing LH and FSH