OB-GYN Revision 12 Flashcards

1
Q
A
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2
Q

Primary amenorrhoea is defined as not starting menstruation by … [2]

What is the definition of secondary amenorrhoea? [1]

A

Primary:
* By 13 years when there is no other evidence of pubertal development
* By 15 years of age where there are other signs of puberty, such as breast bud development

Secondary:
* cessation of menstruation for 3-6 months in women with previously normal and regular menses, or 6-12 months in women with previous oligomenorrhoea

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3
Q

Explain the pathophysiology of hypogonadotropic hypogonadism [3]

A

Deficiency of LH and FSH, leading to deficiency of the sex hormones (oestrogen)
- LH and FSH are produced in the anterior pituitary gland in response to gonadotropin releasing hormone (GnRH) from the hypothalamus.
- Since no gonadotrophins are simulating the ovaries, they do not respond by producing sex hormones (oestrogen).
- Therefore, “hypogonadotropism” causes “hypogonadism

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4
Q

A deficiency of LH and FSH is the result of abnormal functioning of the hypothalamus or pituitary gland. This could be due to what? [+]

A
  • Hypopituitarism (under production of pituitary hormones)
  • Damage to the hypothalamus or pituitary, for example, by radiotherapy or surgery for cancer
  • Significant chronic conditions can temporarily delay puberty (e.g. cystic fibrosis or inflammatory bowel disease)
  • Excessive exercise or dieting can delay the onset of menstruation in girls
  • Constitutional delay in growth and development is a temporary delay in growth and puberty without underlying physical pathology
  • Endocrine disorders such as growth hormone deficiency, hypothyroidism, Cushing’s or hyperprolactinaemia
  • Kallman syndrome
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5
Q

Explain the pathophysiology of hypergonadotropic hypogonadism [3]

A

Hypergonadotropic hypogonadism is where the gonads fail to respond to stimulation from the gonadotrophins (LH and FSH).

Without negative feedback from the sex hormones (oestrogen), the anterior pituitary produces increasing amounts of LH and FSH.

Consequently, you get high gonadotrophins (“hypergonadotropic”) and low sex hormones (“hypogonadism”).

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6
Q

Hypergonadotropic hypogonadism is the result of abnormal functioning of the gonads. This could be due to [3]

A

Previous damage to the gonads (e.g. torsion, cancer or infections such as mumps)
Congenital absence of the ovaries
Turner’s syndrome (XO)

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7
Q

Describe what is meant by congenital adrenal hyperplasia [1]

How does it present in mild [4] and severe cases [1]

A

congenital deficiency of the 21-hydroxylase enzyme:
- underproduction of cortisol and aldosterone, and overproduction of androgens from birth.

Mild cases - typically present at childhood or puberty:
- Tall for age
- Facial hair
* Absent periods (primary amenorrhoea)
* Deep voice
* Early puberty

Severe:
* unwell shortly after birth, with electrolyte disturbances and hypoglycaemia.

NB: In a small number of cases, it involves a deficiency of 11-beta-hydroxylase rather than 21-hydroxylase.

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8
Q

Describe the diagnosis [2] and management [3] of ASS

A

Diagnosis
* buccal smear or chromosomal analysis to reveal 46XY genotype
* after puberty, testosterone concentrations are in the high-normal to slightly elevated reference range for postpubertal boys

Management
* counselling - raise the child as female
* bilateral orchidectomy (increased risk of testicular cancer due to undescended testes)
* oestrogen therapy

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9
Q

Describe what is meant by Androgen insensitivity syndrome [2]

A

X-linked recessive condition due to end-organ resistance to testosterone causing genotypically male children (46XY) to have a female phenotype
- the tissues are unable to respond to androgen hormones (e.g. testosterone), so typical male sexual characteristics do not develop
- It results in a female phenotype, other than the internal pelvic organs.
- Patients have normal female external genitalia and breast tissue.
- Internally there are testes in the abdomen or inguinal canal, and an absent uterus, upper vagina, fallopian tubes and ovaries.

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10
Q

Which structural pathologies can prevent menstruation? [5]

A
  • Imperforate hymen
  • Transverse vaginal septae
  • Vaginal agenesis
  • Absent uterus
  • Female genital mutilation
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11
Q

How do you treat Kallmann’s syndrome? [2]

A

Treatment:
* pulsatile GnRH can be used to induce ovulation and menstruation. This has the potential to induce fertility
* Where pregnancy is not wanted, replacement sex hormones in the form of the combined contraceptive pill may be used to induce regular menstruation and prevent the symptoms of oestrogen deficiency.

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12
Q

Describe the pathophysiology and presentation of Kallmann’s syndrome

A

Kallmann’s syndrome is thought to be caused by failure of GnRH-secreting neurons to migrate to the hypothalamus - causing hypogonadotropic hypogonadism

Presentation:
* ‘delayed puberty’
* hypogonadism, cryptorchidism
* anosmia - clue in many qs
* sex hormone levels are low
* LH, FSH levels are inappropriately low/normal
* patients are typically of normal or above-average height

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13
Q

What is the most common cause of secondary amenorrhea? [1]

What are other common causes [4]

A

Pregnancy is the most common cause
Menopause and premature ovarian failure
Hormonal contraception (e.g. IUS or POP)
Hypothalamic or pituitary pathology
Ovarian causes such as polycystic ovarian syndrome
Uterine pathology such as Asherman’s syndrome
Thyroid pathology
Hyperprolactinaemia

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14
Q

What are pituitary causes of secondary amen. ? [2]

A

Pituitary tumours, such as a prolactin-secreting prolactinoma
Pituitary failure due to trauma, radiotherapy, surgery or Sheehan syndrome

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15
Q

Describe how hyperprolactinaemia influences the hypothalamus and causes amenorrhea?

A
  • High prolactin levels act on the hypothalamus to prevent the release of GnRH.
  • Without GnRH, there is no release of LH and FSH.
  • This causes hypogonadotropic hypogonadism.
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16
Q

What are the most common causes of hyperprolactinaemia? [1]

A

pituitary adenoma secreting prolactin.
- . Often there is a microadenoma that will not appear on the initial scan, and follow up scans are required to identify tumours that may develop later.

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17
Q

What are the features of prolactinomas in women? [4]

A

excess prolactin in women
* amenorrhoea
* infertility
* galactorrhoea
* osteoporosis

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18
Q

Assessment of secondary amenorrhoea involves? [3]

A
  • Detailed history and examination to assess for potential causes
  • Hormonal blood tests
  • Ultrasound of the pelvis to diagnose polycystic ovarian syndrome
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19
Q

s

Desribe the hormonal tests are used to assess secondary amenorrhoea [5]

A

Beta human chorionic gonadotropin (HCG) urine or blood tests are required to diagnose or rule out pregnancy.

Luteinising hormone and follicle-stimulating hormone:
* High FSH suggests primary ovarian failure
* High LH, or LH:FSH ratio, suggests polycystic ovarian syndrome

Prolactin can be measured to assess for hyperprolactinaemia, followed by an MRI to identify a pituitary tumour.

Thyroid stimulating hormone (TSH) can screen for thyroid pathology. This is followed by T3 and T4 when the TSH is abnormal.

Raised testosterone indicates polycystic ovarian syndrome, androgen insensitivity syndrome or congenital adrenal hyperplasia.

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20
Q

TOM TIP: It is worth remembering that women with polycystic ovarian syndrome require a withdrawal bleed every 3 – 4 months to reduce the risk of endometrial hyperplasia and endometrial cancer.

What can be used to do this? [2]

A

Medroxyprogesterone for 14 days, or regular use of the combined oral contraceptive pill, can be used to stimulate a withdrawal bleed.

21
Q

What pathology are those suffering from amenorrhoea more likely to suffer from? [1]

How do you treat this? [1]

A

Patients with amenorrhoea associated with low oestrogen levels are at risk increased risk of osteoporosis. Where the amenorrhoea lasts more than 12 months, treatment is indicated to reduce the risk of osteoporosis:
* Ensure adequate vitamin D and calcium intake
* Hormone replacement therapy or the combined oral contraceptive pill

22
Q

State which type of hypogonadism Turner’s and Kallmans are [2]

A

Turners: Hyper,hypo

Kallman: HypoHypo

23
Q

Clonidine can be used as a non-hormonal treatment for menopausal symptoms.

Which receptors does it work on? [2]

What is the MoA? [1]

Which symptoms is it particularly indicated for in menopause? [2]

A

Clonidine:
- act as an agonist of alpha-2 adrenergic receptors and imidazoline receptors in the brain
- It lowers blood pressure and reduces the heart rate

It can be helpful for vasomotor symptoms and hot flushes, particularly where there are contraindications to using HRT.

24
Q

What are the indications for HRT? [4]

A
  • Replacing hormones in premature ovarian insufficiency, even without symptoms
  • Reducing vasomotor symptoms such as hot flushes and night sweats
  • Improving symptoms such as low mood, decreased libido, poor sleep and joint pain
  • Reducing risk of osteoporosis in women under 60 years
25
Q

Describe the risks of HRT [4]

A
  • Increased risk of breast cancer (particularly combined HRT – oestrogen-only HRT has a lower risk)
  • Increased risk of endometrial cancer unless the women has no uterus
  • Increased risk of venous thromboembolism (2 – 3 times the background risk)
  • Increased risk of stroke and coronary artery disease with long term use in older women in COMBINED HRT (not oestrogen only)

NB The evidence is inconclusive about ovarian cancer, and if there is an increase in risk, it is minimal

26
Q

Describe the relationships between HRT and breast cancer [2]

A

Combined HRT:
- Increases the risk

Oestrogen only:
- Decreases the risk

27
Q

Why are women under 50 with a uterus offered combined HRT? [1]

A

The risk of endometrial cancer is greatly reduced by adding progesterone in women with a uterus

28
Q

There are some essential contraindications to consider in patients wanting to start HRT:

What are they? [7]

A
  • Undiagnosed abnormal bleeding
  • Endometrial hyperplasia or cancer
  • Breast cancer
  • Uncontrolled hypertension
  • Venous thromboembolism
  • Liver disease
  • Active angina or myocardial infarction
  • Pregnancy
29
Q

What are key factors need to ask when assessing if a patient is suitable for HRT? [6]

A

Take a family history to assess the risk of oestrogen dependent cancers (e.g. breast cancer) and VTE

Check the body mass index (BMI) and blood pressure

Ensure cervical and breast screening is up to date

30
Q

Describe the stepwise approach should use to determine what HRT should prescribe [3]

A

Step 1: Do they have local or systemic symptoms?
* Local symptoms: use topical treatments such as topical oestrogen cream or tablets
* Systemic symptoms: use systemic treatment – go to step 2

Step 2: Does the woman have a uterus?
* No uterus: use continuous oestrogen-only HRT
* Has uterus: add progesterone (combined HRT) – go to step 3

Step 3: Have they had a period in the past 12 months?
* Perimenopausal: give cyclical combined HRT
* Postmenopausal (more than 12 months since last period): give continuous combined HRT

31
Q

The Mirena coil is licensed for [] years for endometrial protection, after which time it needs replacing

A

The Mirena coil is licensed for four years for endometrial protection, after which time it needs replacing

32
Q

How would you describe how the insertion of Mirena coil might affect patients? [2]

A

It can cause irregular bleeding and spotting in the first few months after insertion. This usually settles with time and many women become amenorrhoeic.

33
Q

Describe the differences between C19 and C21 progesterones [2]
What are they more likely to be indicated for? [2]

A

C19 progestogens are derived from testosterone, and are more “male” in their effects.
- Examples are norethisterone, levonorgestrel and desogestrel.
- These may be helpful for women with reduced libido.

C21 progestogens are derived from progesterone, and are more “female” in their effects.
- Examples are progesterone, dydrogesterone and medroxyprogesterone.
- These may be helpful for women with side effects such as depressed mood or acne.

34
Q

TOM TIP: The key to HRT is to remember the principles, so that you can counsel women and look up the specific regimes when required.

The best way of delivering oestrogen is with [], due to the reduced risk of venous-thromboembolism.

The best way of providing progesterone is with an []

A

TOM TIP: The key to HRT is to remember the principles, so that you can counsel women and look up the specific regimes when required.

The best way of delivering oestrogen is with patches, due to the reduced risk of venous-thromboembolism.

The best way of providing progesterone is with an intrauterine device, for example, the Mirena coil. The coil has the added benefits of contraception and treating heavy menstrual periods. Additionally, women will not experience progestogenic side effects.

35
Q

offer vaginal [] to women with urogenital atrophy (including those on systemic HRT) and continue treatment for as long as needed to relieve symptoms

A

offer vaginal oestrogen to women with urogenital atrophy (including those on systemic HRT) and continue treatment for as long as needed to relieve symptoms

36
Q

You are being asked to counsel someone to see if they are suitable for HRT.

What questions what you first ask them? [+]

A

Screen for contraindications: ‘I need to see if it’s appropriate for you’:
- Age
- Confirm menopaus if possible
- Discuss symptoms
- PV bleeding - ask about regularity if still occuring; LMP if not; post-coital bleeding
- PE? Stroke?MI?
- Oestrogen dependent cancers (breast / endometrial?)
- Uterus present?

37
Q

You’ve been asked to counsel someone about HRT.

How would you explain what the menopause is and why its occurring? [4]

A

Explain what the menopause is:
- TIme when menstrual periods cease and women can’t get pregnant
- Ovaries run out of follicles and this results in reduced oestrogen production by ovaries
- Oestrogen plays a key role in regulating reproductive system - but can impact mood etc
- Symptoms can last for 4 years on average

38
Q

You’ve been asked to counsel someone about HRT.

Explain how HRT works [1]

A

Replaces oestrogen that isn’t being produced anymore and progesterone that isn’t produced because of follicles not being produced

39
Q

You’ve been asked to counsel someone about HRT.

Explain the risks vs benefits of HRT

A
40
Q

You’ve been asked to counsel someone about HRT.

You have discussed the menopause, types of HRT and their risks / benefits.

What else would should you discuss? [2]

A

Discuss contraception:
- HRT is not contraception - women are potentially still fertile for a year (>50) or two years (< 50) from menopause
- Need to use either barrier methods, POP alongside HRT or Mirena coil (can be used as the P part of HRT - but only lasts for 4 years for HRT)

Discuss alternatives:
- Mood: CBT & antidepressants
- Vasomotor symptoms: SSRIS & clonidine
- Vaginal dryness: Lubricants
- Irregular periods: Mirena coil

41
Q

If you switch between types of HRT, what is the normal range for bleeding to occur in? [1]

A

Within 3 months of changing

42
Q

Describe the differences in symptoms from perimenopause –> early menopause –> menopause [+]

A
43
Q

You suspect menopause in someone under 45.

How would you test for this? [1]

A

Measure FSH
* FSH >30 IU/l (>25 IU/l if < 40 years)
* 2 samples >4 weeks apart

44
Q

What is a really important non-HRT use for menopause? [1]

A
45
Q

Clonidine is one non-hormonal treatment that can be used for vasomotor symptoms.

Explain how another drug can be used

A

Fezolinetant
- Neurokinin 3 receptor antagonist
- Acts at level of hypothalamus on temp regulation

46
Q

What are three unlicensed drugs that can be used to treat vasomotor symptoms? [3]

A

SSRIs/SNRI (venlafaxine)
* licensed for depression
* SEs dry mouth, nausea, constipation, weight gain

Oxybutynin
* licensed for overactive bladder
* SEs dry mouth, dry eyes, nausea, diarrhoea

Gabapentin (Controlled drug)
* Licensed for neuropathic pain and epilepsy
* SEs dizziness, fatigue, tremor, weight gain

47
Q

Describe the risk of oestrogen only vs oestrogen and progesterone HRT for endometrial cancer [2]

A

Endometrial cancer:
* Oestrogen only: increased risk
* O & P: decreased risk

48
Q

Which types of HRT specifically increase the risk of VTE? [2]

A

Oral oestrogen
Oral synthetic progesterones

49
Q

How long can you continue taking HRT? [1]

A

As long as want, no cut off date