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Woman's Health > 2.1 Infertility in Women > Flashcards

2.1 Infertility in Women Flashcards

1
Q

How can temperature be used to monitor ovulation?

A
  • Rise in basal body temperature 1-2 days after LH surge (indicate ovulation)
  • Basal body temperature is lower in the proliferative phase:
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2
Q

How can be urinary LH be used to monitor ovulation?

A

Serum LH levels rise 24 – 36 hours before ovulation:
• Urinary LH (surrogate marker for serum LH) is measured using the ovulation kit
• Can be tested daily from day 10 until positive (coitus is advised 12 – 24 hours after to maximise pregnancy chances)

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3
Q

How can serum progesterone be used to monitor ovulation?

A

Blood test detects rise in serum progesterone in mid-luteal phase

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4
Q

How can follicular tracking be used to monitor ovulation?

A

Document the size and growth of ovarian follicles

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5
Q

How can cervical mucus be used to monitor ovulation?

A

Nature and consistency of the cervical mucus changes cyclically:
• Follicular phase: minimal thick mucus forming a complex mesh in the cervical canal (proliferation of cervical glands)
• Just before ovulation: high quantity thin stringy mucus (Spinnbarkeit) (due to sudden surge in oestrogen)
• After ovulation: thick impenetrable mucus (progesterone alters nature of the mucus)

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6
Q

Fertilisation is the fusion of the sperm (lifespan ____________; lasting up to 5 days depending on the environment) and the oocyte (lifespan ___________):
• Most pregnancies are when coitus occurs within the ________ prior to ovulation
• Oocyte enters the ampulla of the Fallopian tube within ______________ of ovulation → fertilisation occurs within the Fallopian tube
• Fallopian tube holds the fertilised oocyte (zygote) for _________ (allows some time for the endometrium to prepare for implantation of the embryo)
• Embryo enters the uterine cavity ~3 days after ovulation → implantation occurs 1 – 3 days after entry into the uterine cavity

A

48 – 72 hours;

12 – 24 hours;

3 day interval;

15 – 20 minutes;

~80 hours

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7
Q

What are the female factors causing infertility?

A
  • Female factors include ovarian causes (most common), tubal causes, uterine/vaginal causes, cervical causes (e.g. congenital malformation, surgical trauma → cervical stenosis and inability to produce normal mucus)
  • Other factors include chromosomal balanced translocation, endometriosis, and autoimmune causes (antiphospholipid syndrome → increased risk of early pregnancy loss, coeliac disease)
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8
Q

When is anovulation physiological?

A

re-puberty, pregnancy/lactation, and post-menopause

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9
Q

what does anovulation present with?

A

irregular menses, oligomenorrhoea, or amenorrhoea

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10
Q

What are the causes of hypogonadotrophic, hypooestrogenic anovulation?

A

Class I (Hypothalamic Causes)

  • Immaturity of HPG axis (usually occurs transiently around the onset of menarche or perimenopausal decline)
  • Kallmann syndrome
  • Hypothalamic tumours (craniopharyngiomas, metastatic tumours)
  • Autoimmune diseases (lymphocytic hypophysitis)
  • Infiltrative diseases (sarcoidosis)
  • Intense exercise/stress/eating disorders → treat underlying cause

Pituitary causes

  • Hyperprolactinaemia
  • External damage (Trauma/surgery to the hypothalamic stalk, Radiation to hypothalamic/pituitary area)
  • Sheehan’s syndrome (Anterior pituitary infarction after massive postpartum haemorrhage (PPH))
  • Pituitary apoplexy (Sudden haemorrhage or impaired blood supply into pituitary gland due to a pituitary adenoma → increased pressure)
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11
Q

What are the causes of normogonadotrophic, normooestrogenic anovulation?

A

PCOS

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12
Q

What are the causes of hypergonadotrophic, hypooestrogenic anovulation?

A
  • Chromosomal: Turner syndrome (45XO), other X chromosomal deletions / inversions / duplications / translocations, fragile X syndrome
  • Autoimmune: Includes SLE, myasthenia gravis
  • Iatrogenic: Radiation, chemotherapy, surgery (for ovaries/in pelvic region)
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13
Q

What are the symptoms of hyperprolactinemia?

A

galactorrhoea, amenorrhoea, subfertility

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14
Q

How does hyperprolactinaemia cause anovulation?

A

High prolactin → stimulates dopamine → decreases GnRH → decreases FSH/LH → no LH surge → anovulation

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15
Q

What are the symptoms of sheehan’s syndrome or pituitary apoplexy?

A

adrenal insufficiency (lethargy, anorexia, weight loss, diabetes insipidus, hypothyroidism, Addisonian crisis → giddiness, vomiting, abdominal pain, hypotension, hyponatraemia with hyperkalaemia), hypogonadism (amenorrhoea, lactation failure)

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16
Q

What are the acute symptoms of pituitary apoplexy?

A

sudden-onset headache behind the eyes or around the temples (most common) associated with N/V, meningitis, bitemporal hemianopia (pressure on optic chiasm), cavernous sinus thrombosis

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17
Q

What is the pathophysiology of PCOS?

A
  • Uncertain mechanism (with genetic component) leading to excessive LH release or hyperinsulinaemia → hyperandrogenic state of ovaries
  • Elevated androgen levels cause early development of many small pre-ovulatory follicles → premature luteinisation → maturation arrest at large antral follicular stage (“cysts” are a misnomer) → oligo/anovulation
18
Q

What are the presentations of PCOS?

A

Patients with PCOS often present asymptomatically (incidental finding on ultrasound): • Classic triad (remember PcOS): oligomenorrhoea (with anovulatory cycles), polycystic appearance (enlarged ovary with numerous small peripheral follicles in a “string of pearls” distribution on ultrasound), abnormal secondary sexual characteristics (hyperandrogenism → hirsutism, weight gain, acne → secondary to high virilising hormones and low SHBG)
• Metabolic syndrome (diabetes mellitus/insulin resistance) → increased risk of CVD
• Subfertility (due to anovulation

19
Q

What is the diagnostic criteria for PCOS?

A

The first thing to do in the diagnosis of PCOS must be the exclusion of other hyperandrogenic causes → then fulfilment of 2 out of 3 of the Rotterdam criteria (diagnosis of exclusion):

  1. Oligo/anovulation
  2. Hyperandrogenism: clinical (hirsutism, male pattern alopecia) or biochemical (raised free testosterone levels)
  3. Polycystic ovary on ultrasound scan
20
Q

What is the treatment for PCOS?

A
  • Lifestyle modification: First-line treatment (diet, exercise, weight loss)
  • Cyclical COCP/ progestestrone: Ensure withdrawal bleed at least once every 3 months to prevent endometrial hyperplasia/cancer → oestrogen reduces androgen levels in the body
  • Symptomatic treatment: Medical treatment for acne/hirsutism/alopecia:
    • OCP: decrease androgen production
    • Spironolactone: blocks androgenic effects on skin (contraindicated in pregnancy/planning conception)
  • Diabetics screen
21
Q

When is diabetes screen done in PCOS patients?

A
  • During pregnancy (24 – 28 weeks): gestational DM (GDM)
  • Overweight (BMI ≥ 25kg/m2)
  • Not overweight but with additional risk factors (age > 40, personal history of GDM, family history of T2DM
22
Q

What are the medications if patient with PCOS is keen for pregnancy?

A
  • Clomiphene: oral anti-oestrogen medication

* Gonadotrophin/GnRH analogues (e.g. goserelin)

23
Q

what are endocrine causes of infertility?

A
  • Hormone-producing tumour of the adrenal gland/ovaries
  • Cushing’s disease (hypercortisolism)
  • Congenital adrenal hyperplasia (CAH)
  • Androgen insensitivity syndrome (AIS)
  • Poorly controlled thyroid diseases/diabetes mellitus
24
Q

what are tubal causes (pathologies/ iatrogenic causes of fallopian tubes) that cause infertility?

A
  • tubal disease: prevents sperm from reaching the egg for fertilisation and transport of the embryo into the uterine cavity → causes ectopic tubal pregnancies
  • Blockage: Prevents proper transport of the egg and sperm
  • hydrosalpinx
  • tubal ligation
25
Q

What is the definition of hydrosalpinx?

A

Swollen fluid-filled tubes causing obstruction of sperm migration:
• Retrograde flow of tubal contents into the endometrial cavity creates a hostile environment for embryo implantation
• May cause chronic pelvic pain

26
Q

What are the causes of tubal diseases?

A
  • Pelvic inflammatory disease (PID) caused by Chlamydia trachomatis (most common cause) and Neisseria gonorrhoeae
  • Severe endometriosis (see below)
  • Iatrogenic causes (history of salpingectomy, ascending infection from uterine instrumentation/IUD insertion, Filshie clip application (for tubal ligation))
  • Adhesions from previous surgeries
  • Non-tubal infections (e.g. appendicitis, IBS)
  • Pelvic TB (rare)
27
Q

what is the surgical procedure to treat proximal tubal blockages?

A

Clearing proximal blockages of Fallopian tubes with a cannula via hysteroscopy (examining the interior of uterus with hysteroscope

28
Q

what is the surgical procedure to treat proximal tubal blockages?

A

Tubal cannulation: Clearing proximal blockages of Fallopian tubes with a cannula via hysteroscopy (examining the interior of uterus with hysteroscope

29
Q

what is the surgical procedure to treat distal tubal blockages?

A

Neosalpingostomy: Surgery to drain and unblock distal tube disease → suture edges to keep the tubes open

30
Q

what is the surgical procedure to treat hydrosalpinx?

A

Salpingestomy: of Fallopian tubes (increases success of IVF by 50%)

31
Q

Infertility may result from impaired implantation of the embryo due to mechanical issues or reduced endometrial receptivity. What are these causes?

A

Uterine fibroids, Endometrial polyps, endometrial adhesions (Asherman’s syndrome), endometriosis

32
Q

What is endometriosis?

A

Endometriosis is the deposition of endometrial tissue outside of the uterus (different from adenomyosis → deposition in the myometrium – still part of the uterus)

33
Q

Where is endometriosis found?

A

Commonly found in the pelvis (ovaries, ovarian fossae, uterosacral ligaments, pouch of Douglas) → may range from mild to severe

34
Q

How does endometriosis decrease fertility?

A

anatomic distortion (from pelvic adhesions), endometrioma formation (damages ovarian tissue), release of cytokines and growth factors (impede normal ovulation and fertilisation, and implantation)

35
Q

What are the causes of endometriosis?

A
  1. Retrograde menstruation and implantation theory (most widely accepted): endometrial tissue shed is transported via Fallopian tubes into peritoneal cavity → implants on the surfaces of pelvic organs
  2. Coelomic metaplasia theory: spontaneous metaplastic change in mesothelial cells derived from the coelomic epithelium
  3. Vascular/lymphatic dissemination of endometrial cells
  4. Direct transplantation of endometrial tissue
36
Q

What are the symptons of endometriosis?

A
  • gynaeocological: dysmenorrhoea, non-cyclical pelvic pain, deep dyspareunia, fatigue, infertility
  • non gynaecological: dyschezia (constipation associated with defective defecation reflex), dysuria, haematuria, cyclical per-rectal bleeding, shoulder pain
37
Q

How is the management of pain treated for endometriosis?

A
  • Analgelsia: NSAIDs (ibuprofen, aspirin etc.)
  • Hormonal medication (little evidence): COCP, progestogens, LNG-IUS (Mirena®), GnRH agonists
  • Surgery: For patients with failed medical management
38
Q

What are the causes of developmental defects of the Mullerian system (Fallopian tubes, uterus, cervix, upper third of the vagina) may also cause female infertility?

A

Mayer-Rokitansky-Küster-Hauser (MRKH) syndrome: very rare embryonic growth failure of the Mullerian duct → agenesis or underdevelopment of vagina, uterus, or both

39
Q

What are the causes of developmental defects of the Mullerian system (Fallopian tubes, uterus, cervix, upper third of the vagina) may also cause female infertility?

A
  • Mayer-Rokitansky-Küster-Hauser (MRKH) syndrome: very rare embryonic growth failure of the Mullerian duct → agenesis or underdevelopment of vagina, uterus, or both
  • Lateral fusion defects
  • Vertical fusion defects
40
Q

What kind of lateral fusion defects are the most common?

A

septate, arcuate, uni/bicornuate uterus, uterus didelphys → double uterus with two separate cervices

41
Q

What are vertical fusion defects?

A

Presence of vaginal septum (transverse/longitudinal), cervical agenesis/dysgenesis

Woman's Health (29 decks)

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